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157 | 1 | Mechanisms of glycolytic inhibition in ischemic rat hearts. | MEDLINE | Manual | NLM | The mechanisms of glycolytic inhibition in ischemic myocardium were investigated in the isolated, perfused rat heart. Glycolysis was inhibited at the level of glyceraldehyde-3-phosphate dehydrogenase. The major factors that accounted for the glycolytic inhibition in the ischemic heart compared with the anoxic heart appeared to be higher tissue levels of lactate and H+ in the ischemic tissue. Increased extracellular pH inhibited glycolysis in anoxic and hypoxic hearts much more readily than it did in aerobic hearts. However, maintenance of both extracellular and intracellular pH caused only a modest acceleration of glycolysis in ischemic hearts. Accumulation of tissue lactate and inhibition of glycolysis were directly proportional to the reduction in coronary bloow flow in both anoxic and ischemic hearts. At intracellular lactate concentrations between 15 and 20 mM, glycolysis was inhibited under both conditions. Addition of either 10, 20, or 40 mM lactate to the perfusate inhibited glycolysis in aerobic, anoxic, and ischemic hearts. The effect of lactate did not appear to be mediated through changes in intracellular pH. It is concluded that accumulation of lactate represents a major factor in the inhibition of glycolysis that develops in ischemic hearts. | Circulation research | 0009-7330 | Print | 37 | 6 | Print | 1,975 | Dec | null | 742-51 | M J Rovetto (MJ); W F Lamberton (WF); J R Neely (JR) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Insulin (Registry: 0, UI: D007328); Lactates (Registry: 0, UI: D007773); Glucose (Registry: IY9XDZ35W2, UI: D005947) | Animals (UI: D000818, Major: No); Blood Flow Velocity (UI: D001783, Major: No); Coronary Circulation (UI: D003326, Major: Yes); Coronary Disease (UI: D003327, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Extracellular Space (UI: D005110, Major: No); Glucose (UI: D005947, Major: No) - Qualifiers: administration & dosage (UI: Q000008, Major: No); Glycolysis (UI: D006019, Major: Yes); Heart (UI: D006321, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); In Vitro Techniques (UI: D066298, Major: No); Insulin (UI: D007328, Major: No) - Qualifiers: administration & dosage (UI: Q000008, Major: No); Intracellular Fluid (UI: D007424, Major: No); Lactates (UI: D007773, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Male (UI: D008297, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Perfusion (UI: D010477, Major: No); Rats (UI: D051381, Major: No) | Animals|Blood Flow Velocity|Coronary Circulation|Coronary Disease|Extracellular Space|Glucose|Glycolysis|Heart|Hydrogen-Ion Concentration|In Vitro Techniques|Insulin|Intracellular Fluid|Lactates|Male|Myocardium|Perfusion|Rats | |||metabolism (1)||administration & dosage (0)|||||administration & dosage (0)||pharmacology (0)||metabolism (1)|| | 0|0|1|0|0|0|1|0|0|0|0|0|0|0|0|0|0 | null | 1976-02-26 | 2019-07-06 | pubmed: 1975-12-1; medline: 1975-12-1 0:1; entrez: 1975-12-1 0:0 | pubmed: 157; doi: 10.1161/01.res.37.6.742 | Myocardial Ischemia | ['Coronary Disease'] |
404 | 1 | Arterialization of the coronary veins in diffuse coronary arteriosclerosis. | MEDLINE | Manual | NLM | Since the coronary veins and capillaries are not involved with arteriosclerotic disease the authors performed experimental, and afterwards, clinical total and selective coronary vein arterialization. Acute myocardial ischaemia created for instance by ligation of the anterior descending branch, was treated by an internal mammary artery to regional coronary vein anastomosis. In 21 patients the selective arterialization of the ""Vena cordis magna"" or of ""Vena cordis media"", and total arterialization of the coronary sinus was performed. The clinical improvement and follow-up studies seem to be promising in the treatment of patients with advanced diffuse heavy coronary arteriosclerosis. In acute myocardial ischaemia with coronarographically localized coronary occlusion, the aim of regional vein arterialization is to minimize the area of infarction. | The Journal of cardiovascular surgery | 0021-9509 | Print | 16 | 5 | Print | null | null | null | 520-5 | J W Moll (JW); A J Dziatkowiak (AJ); M Edelman (M); W Iljin (W); E Ratajczyk-Pakalska (E); K Stengert (K) | Journal Article (D016428) | null | Adult (UI: D000328, Major: No); Aged (UI: D000368, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: surgery (UI: Q000601, Major: Yes); Coronary Vessels (UI: D003331, Major: No) - Qualifiers: surgery (UI: Q000601, Major: Yes); Female (UI: D005260, Major: No); Follow-Up Studies (UI: D005500, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Methods (UI: D008722, Major: No); Middle Aged (UI: D008875, Major: No); Myocardial Revascularization (UI: D009204, Major: No); Veins (UI: D014680, Major: No) - Qualifiers: surgery (UI: Q000601, Major: No) | Adult|Aged|Coronary Disease|Coronary Vessels|Female|Follow-Up Studies|Humans|Male|Methods|Middle Aged|Myocardial Revascularization|Veins | ||surgery (1)|surgery (1)||||||||surgery (0) | 0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-02-09 | 2023-08-15 | pubmed: 1975-9-1; medline: 1975-9-1 0:1; entrez: 1975-9-1 0:0 | pubmed: 404 | Myocardial Ischemia | ['Coronary Disease'] |
480 | 1 | Recognition and significance of maternogenic fetal acidosis during intensive monitoring of labor. | MEDLINE | Manual | NLM | FHR monitoring and microanalysis of fetal blood are mutually complementary procedures, and optimal knowledge of the fetal state is achieved by making use of both, the former for the preliminary screening of all cases at risk and the latter for the purpose of deciding on obstetric management where pathological changes are evident in the FHR. The major difficulty in obtaining a precise value for the fetal acid-base balance lies in the occurence of ""falsely abnormal"" cases, i.e. cases in which the fetal pH falls during labor but the clinical condition at birth is good (APGAR greater than or equal to 7). In our own series the incidence of such cases among fetuses at risk was 11.2% (Tab. I). In the majority of these cases the fetal acidosis is thought to be a result of increased metabolic acidosis in the mother (maternogenic fetal metabolic acidosis). The importance of the maternogenic fetal acidosis during labor lies in the fact that unless it is recognised, rapid extraction of the fetus will appear necessary on clinical grounds, although it is in fact unnecessary, since this form of acidosis has no adverse effect on the fetus. Various parameters have been proposed for the differential diagnosis of the maternogenic fetal acidosis. These include the feto-maternal difference in base deficit (F/M deltaBD), the materno-fetal differences in pHqu 40 (M/F deltapHqu 40) the materno-fetal difference actual pH (M/F actual deltapH), and the materno-fetal difference in base deficit of the extra-cellular fluid (M/F deltaBDHb5). A critical analysis of these parameters has been carried out on the results of microtests performed during a 5 year period (1968-1972) at the First Clinic of Obstetrics and Gynecology of Milan University. The cases comprised 59 regarded as normal (normal course of pregnancy, spontaneous commencement of labor at term, clear amniotic fluid, regular FHR, spontaneous birth, APGAR at 90 sec between 8 and 10, weight at birth greater than 2500 g), and 335 considered to be at risk (maternal disease, presence of meconium stained amniotic fluid and/or abnormal changes in FHR). In all of these cases the FHR was recorded by cardiotokography, and the tracings were interpreted according to HON. Microsamples of blood were taken from both mother and fetus during labor and the following determinations were carried out: actual pH, pHqu 40, Hb concentration, hemoglobin oxygen saturation, base deficit Hb5 (BDHb5). The maternofetal differences were then calculated. The same determinations were carried out on samples of maternal blood and of arterial and venous cord blood taken immediately after delivery. The clinical condition of the infant was evaluated by the APGAR score at 90 seconds after birth. | Journal of perinatal medicine | 0300-5577 | Print | 3 | 1 | Print | 1,975 | null | null | 53-67 | G D Roversi (GD); V Canussio (V); M Spennacchio (M) | Journal Article (D016428) | Hemoglobins (Registry: 0, UI: D006454) | Acid-Base Equilibrium (UI: D000136, Major: No); Acidosis (UI: D000138, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: Yes); Apgar Score (UI: D001034, Major: No); Bradycardia (UI: D001919, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); Electrocardiography (UI: D004562, Major: No) - Qualifiers: methods (UI: Q000379, Major: No); Female (UI: D005260, Major: No); Fetal Distress (UI: D005316, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: Yes); Fetal Heart (UI: D005318, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Heart Rate (UI: D006339, Major: No); Hemoglobins (UI: D006454, Major: No); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Infant, Newborn (UI: D007231, Major: No); Maternal-Fetal Exchange (UI: D008431, Major: Yes); Monitoring, Physiologic (UI: D008991, Major: No); Obstetric Labor Complications (UI: D007744, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: Yes); Pregnancy (UI: D011247, Major: No); Uterine Contraction (UI: D014590, Major: No) | Acid-Base Equilibrium|Acidosis|Apgar Score|Bradycardia|Electrocardiography|Female|Fetal Distress|Fetal Heart|Heart Rate|Hemoglobins|Humans|Hydrogen-Ion Concentration|Infant, Newborn|Maternal-Fetal Exchange|Monitoring, Physiologic|Obstetric Labor Complications|Pregnancy|Uterine Contraction | |diagnosis (1)||diagnosis (0)|methods (0)||diagnosis (1)|physiopathology (0)||||||||diagnosis (1)|| | 0|0|0|0|0|0|0|0|0|0|0|0|0|1|0|0|0|0 | null | 1976-02-19 | 2019-09-18 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 480; doi: 10.1515/jpme.1975.3.1.53 | Arrhythmias, Cardiac | ['Bradycardia'] |
741 | 1 | Role of cardiovascular and ionic changes in pathogenesis and prevention of isoprenaline-induced cardiac necrosis. | MEDLINE | Manual | NLM | Blood pressure, heart rate, oxygen uptake, and blood values of PO2, PCO2, and pH were studied in unanesthetized rats for 8 hours. After a cardiotoxic dose of 20 mg/kg isoprenaline, s.c., blood pressure fell from 117 to 72 mm Hg, heart rate accelerated from 326 to 497 beats/minute, and cardiac work diminished by about 15%. Metabolic rate increased by about 80%, blood values of PO2 rose, and those of PCO2 fell somewhat, whereas blood pH dropped from 7.48 to 7.38, indicating metabolic acidosis. Propranolol (40 mg/kg, i.p.) and verapamil (50 mg/kg, i.p.), both of which almost completely prevented isoprenaline-induced cardiac necroses, inhibited the chronotropic and calorigenic actions of isoprenaline by about 50%. While propranolol inhibited the depressor effect of isoprenaline completely, verapamil enhanced it: blood pressure fell to 46 mm Hg. Isoprenaline-induced fall of blood pH was not prevented by either propranolol or verapamil. Decrease of blood pH and cardionecrotisation were enhanced when isoprenaline was given together with 4.8 g/kg ethanol, p.o. In conclusion, hemodynamic actions of isoprenaline, especially hypotension, seem to be nonessential for the production of cardiac necroses. Strong acidification can aggravate the cardiotoxicity of isoprenaline. | Recent advances in studies on cardiac structure and metabolism | 0363-5872 | Print | 6 | null | Print | 1,975 | null | null | 135-42 | O Strubelt (O); C P Siegers (CP) | Journal Article (D016428) | Carbon Dioxide (Registry: 142M471B3J, UI: D002245); Propranolol (Registry: 9Y8NXQ24VQ, UI: D011433); Verapamil (Registry: CJ0O37KU29, UI: D014700); Isoproterenol (Registry: L628TT009W, UI: D007545); Oxygen (Registry: S88TT14065, UI: D010100) | Animals (UI: D000818, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Carbon Dioxide (UI: D002245, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Cardiomyopathies (UI: D009202, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: Yes); pathology (UI: Q000473, Major: No); physiopathology (UI: Q000503, Major: No); prevention & control (UI: Q000517, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); pharmacology (UI: Q000494, Major: Yes); Male (UI: D008297, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Necrosis (UI: D009336, Major: No); Oxygen (UI: D010100, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Oxygen Consumption (UI: D010101, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Propranolol (UI: D011433, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Rats (UI: D051381, Major: No); Verapamil (UI: D014700, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No) | Animals|Blood Pressure|Carbon Dioxide|Cardiomyopathies|Heart Rate|Hydrogen-Ion Concentration|Isoproterenol|Male|Myocardium|Necrosis|Oxygen|Oxygen Consumption|Propranolol|Rats|Verapamil | |drug effects (0)|blood (0)|chemically induced (1); pathology (0); physiopathology (0); prevention & control (0)|drug effects (0)||antagonists & inhibitors (0); pharmacology (1)||metabolism (0)||blood (0)|drug effects (0)|therapeutic use (0)||therapeutic use (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-02-27 | 2013-11-21 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 741 | Cardiomyopathies | [] |
742 | 1 | Alterations in norepinephrine pattern in the damaged myocardium in the rat. | MEDLINE | Manual | NLM | In the albino rat, the evolvement of myocardial necrosis induced by a single injection of ISO was accompanied by a fall in total NE. Pretreatment with propranolol and pargyline protected against ISO-induced necrosis and myocardial hypertrophy, but did not influence the ISO-induced depletion of NE stores. The depletion of NE stores is not due to impairment in synthesis or increased intraneuronal metabolism of NE since, in ISO-treated rats, neither cardiac tyrosine hydroxylase activity nor MAO activity was altered. The decrease in endogenous NE is not due to a defect in the storage of NE. The ability of myocardium to take up and store NE returned to normal within 48 hours, whereas endogenous levels returned to normal within 5 days, even in the presence of demonstrable necrosis. Thus, there is lack of correlation between chemical and morphological changes, since catecholamine depletion occurred in the absence of morphologically demonstrable tissue injury, and the function of the adrenergic neuron returns to normal in the presence of demonstrable necrosis. | Recent advances in studies on cardiac structure and metabolism | 0363-5872 | Print | 6 | null | Print | 1,975 | null | null | 159-65 | B Bhagat (B); J M Sullivan (JM); N S Dhalla (NS) | Journal Article (D016428) | Pargyline (Registry: 9MV14S8G3E, UI: D010293); Propranolol (Registry: 9Y8NXQ24VQ, UI: D011433); Tyrosine 3-Monooxygenase (Registry: EC 1.14.16.2, UI: D014446); Monoamine Oxidase (Registry: EC 1.4.3.4, UI: D008995); Isoproterenol (Registry: L628TT009W, UI: D007545); Norepinephrine (Registry: X4W3ENH1CV, UI: D009638) | Animals (UI: D000818, Major: No); Cardiomegaly (UI: D006332, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); Cardiomyopathies (UI: D009202, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); metabolism (UI: Q000378, Major: Yes); pathology (UI: Q000473, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Male (UI: D008297, Major: No); Monoamine Oxidase (UI: D008995, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: enzymology (UI: Q000201, Major: No); metabolism (UI: Q000378, Major: No); Necrosis (UI: D009336, Major: No); Norepinephrine (UI: D009638, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Pargyline (UI: D010293, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Propranolol (UI: D011433, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Rats (UI: D051381, Major: No); Tyrosine 3-Monooxygenase (UI: D014446, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No) | Animals|Cardiomegaly|Cardiomyopathies|Isoproterenol|Male|Monoamine Oxidase|Myocardium|Necrosis|Norepinephrine|Pargyline|Propranolol|Rats|Tyrosine 3-Monooxygenase | |chemically induced (0)|chemically induced (0); metabolism (1); pathology (0)|pharmacology (1)||metabolism (0)|enzymology (0); metabolism (0)||metabolism (1)|pharmacology (0)|pharmacology (0)||metabolism (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-02-27 | 2013-11-21 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 742 | Cardiomyopathies | [] |
743 | 1 | Prevention of myocardial Ca overload and necrotization by Mg and K salts or acidosis. | MEDLINE | Manual | NLM | The crucial point in the pathogenesis of isoproterenol-induced myocardial necrotization is an abundant intracellular Ca accumulation leading to high energy phosphate exhaustion. Accordingly, in the early stage of the isoproterenol-induced necrotization process, the onset of ATP and creatine phosphate breakdown strictly parallels the acute Ca gain. In this type of necrosis, the Mg losses from the myocardium appear as a concomitant phenomenon. The hearts can be protected against the deleterious Ca overload and necrotization by increasing the plasma concentration of Mg, K, or H ions in order to counterbalance Ca according to the ration (see article). On the other hand, if Mg, K, or H ion concentrations are too low, isoproterenol-induced Ca uptake and myocardial lesions are potentiated. | Recent advances in studies on cardiac structure and metabolism | 0363-5872 | Print | 6 | null | Print | 1,975 | null | null | 33-42 | J Janke (J); A Fleckenstein (A); B Hein (B); O Leder (O); H Sigel (H) | Journal Article (D016428) | Phosphocreatine (Registry: 020IUV4N33, UI: D010725); Adenosine Triphosphate (Registry: 8L70Q75FXE, UI: D000255); Magnesium (Registry: I38ZP9992A, UI: D008274); Isoproterenol (Registry: L628TT009W, UI: D007545); Potassium (Registry: RWP5GA015D, UI: D011188); Calcium (Registry: SY7Q814VUP, UI: D002118) | Adenosine Triphosphate (UI: D000255, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Animals (UI: D000818, Major: No); Calcium (UI: D002118, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: Yes); metabolism (UI: Q000378, Major: No); Cardiomyopathies (UI: D009202, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); metabolism (UI: Q000378, Major: No); prevention & control (UI: Q000517, Major: Yes); Dose-Response Relationship, Drug (UI: D004305, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); Magnesium (UI: D008274, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Necrosis (UI: D009336, Major: No); Phosphocreatine (UI: D010725, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Potassium (UI: D011188, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes); Rats (UI: D051381, Major: No) | Adenosine Triphosphate|Animals|Calcium|Cardiomyopathies|Dose-Response Relationship, Drug|Hydrogen-Ion Concentration|Isoproterenol|Magnesium|Myocardium|Necrosis|Phosphocreatine|Potassium|Rats | metabolism (0)||antagonists & inhibitors (1); metabolism (0)|chemically induced (0); metabolism (0); prevention & control (1)|||antagonists & inhibitors (0)|pharmacology (0); therapeutic use (1)|metabolism (0)||metabolism (0)|pharmacology (0); therapeutic use (1)| | 0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-02-27 | 2017-03-22 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 743 | Cardiomyopathies | [] |
1,351 | 1 | Effect of the beta-receptor blocking agent Visken on the action of coumarin. | MEDLINE | Manual | NLM | In a double-blind study, the influence of Visken on the effect of anticoagulant therapy with Marcoumar was examined. In comparison to a placebo group, neither any influence on the Quick time, nor any increased tendency to haemorrhage bleeding could be detected. | International journal of clinical pharmacology and biopharmacy | 0340-0026 | Print | 12 | 4 | Print | 1,975 | Dec | null | 458-60 | H Vinazzer (H) | Clinical Trial (D016430); Controlled Clinical Trial (D018848); Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Anticoagulants (Registry: 0, UI: D000925); Coumarins (Registry: 0, UI: D003374); Placebos (Registry: 0, UI: D010919) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Age Factors (UI: D000367, Major: No); Aged (UI: D000368, Major: No); Anticoagulants (UI: D000925, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Arterial Occlusive Diseases (UI: D001157, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Blood Coagulation (UI: D001777, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: Yes); Blood Coagulation Disorders (UI: D001778, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Body Height (UI: D001827, Major: No); Body Weight (UI: D001835, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Coumarins (UI: D003374, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Drug Interactions (UI: D004347, Major: No); Drug Therapy, Combination (UI: D004359, Major: No); Humans (UI: D006801, Major: No); Long-Term Care (UI: D008134, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Placebos (UI: D010919, Major: No); Time Factors (UI: D013997, Major: No) | Adrenergic beta-Antagonists|Age Factors|Aged|Anticoagulants|Arterial Occlusive Diseases|Blood Coagulation|Blood Coagulation Disorders|Body Height|Body Weight|Coronary Disease|Coumarins|Drug Interactions|Drug Therapy, Combination|Humans|Long-Term Care|Male|Middle Aged|Myocardial Infarction|Placebos|Time Factors | pharmacology (1)|||therapeutic use (0)|drug therapy (0)|drug effects (1)|drug therapy (0)|||drug therapy (0)|pharmacology (1)|||||||drug therapy (0)|| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-03-24 | 2004-11-17 | pubmed: 1975-12-1; medline: 1975-12-1 0:1; entrez: 1975-12-1 0:0 | pubmed: 1351 | Myocardial Ischemia | ['Coronary Disease', 'Myocardial Infarction'] |
1,448 | 1 | Defects in the biochemistry of collagen in diseases of connective tissue. | MEDLINE | Manual | NLM | The collagens are the major structural glycoproteins of connective tissues. A unique primary structure and a multiplicity of post-translational modification reactions are required for normal fibrillogenesis. The post-translational modifications include hydroxylation of prolyl and lysyl residues, glycosylation, folding of the molecule into triple-helical conformation, proteolytic conversion of precursor procollagen to collagen, and oxidative deamination of certain lysyl and hydroxylysyl residues. Any defect in the normal mechanisms responsible for the synthesis and secretion of collagen molecules or the deposition of these molecules into extracellular fibers could result in abnormal fibrillogenesis; such defects could result in a connective tissue disease. Recently, defects in the regulation of the types of collagen synthesized and in the enzymes involved in the post-translational modifications have been found in heritable diseases of connective tissue. Thus far, the primary heritable disorders of collagen metabolism in man include lysyl hydroxylase deficiency in Ehlers-Danlos syndrome type VI, p-collagen peptidase deficency in Ehlers-Danlos syndrome type VII, decreased synthesis of type III collagen in Ehlers-Danlos syndrome type IV, lysyl oxidase deficency in S-linked cutis laxa and Ehlers-Danlos syndrome type V, and decreased synthesis of type I collagen in osteogenesis imperfecta. | The Journal of investigative dermatology | 0022-202X | Print | 66 | 02 | Print | 1,976 | Feb | null | 59-79 | J Uitto (J); J R Lichtenstein (JR) | Journal Article (D016428); Research Support, U.S. Gov't, Non-P.H.S. (D013486); Research Support, U.S. Gov't, P.H.S. (D013487); Review (D016454) | Hydroxylysine (Registry: 2GQB349IUB, UI: D006901); Collagen (Registry: 9007-34-5, UI: D003094); Protein-Lysine 6-Oxidase (Registry: EC 1.4.3.13, UI: D008249); Microbial Collagenase (Registry: EC 3.4.24.3, UI: D003012); Hydroxyproline (Registry: RMB44WO89X, UI: D006909) | Aortic Diseases (UI: D001018, Major: No) - Qualifiers: etiology (UI: Q000209, Major: No); Bone and Bones (UI: D001842, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: No); Brain Diseases (UI: D001927, Major: No) - Qualifiers: genetics (UI: Q000235, Major: No); Collagen (UI: D003094, Major: No) - Qualifiers: biosynthesis (UI: Q000096, Major: Yes); metabolism (UI: Q000378, Major: No); Connective Tissue (UI: D003238, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Cutis Laxa (UI: D003483, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); pathology (UI: Q000473, Major: No); Ehlers-Danlos Syndrome (UI: D004535, Major: No) - Qualifiers: genetics (UI: Q000235, Major: No); metabolism (UI: Q000378, Major: No); pathology (UI: Q000473, Major: No); Fascia (UI: D005205, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: No); Genetic Linkage (UI: D008040, Major: No); Homocystinuria (UI: D006712, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Humans (UI: D006801, Major: No); Hydroxylysine (UI: D006901, Major: No) - Qualifiers: biosynthesis (UI: Q000096, Major: No); Hydroxyproline (UI: D006909, Major: No) - Qualifiers: biosynthesis (UI: Q000096, Major: No); urine (UI: Q000652, Major: No); Joints (UI: D007596, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: No); Marfan Syndrome (UI: D008382, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Microbial Collagenase (UI: D003012, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Osteogenesis Imperfecta (UI: D010013, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); pathology (UI: Q000473, Major: No); Protein Biosynthesis (UI: D014176, Major: No); Protein Conformation (UI: D011487, Major: No); Protein-Lysine 6-Oxidase (UI: D008249, Major: No) - Qualifiers: deficiency (UI: Q000172, Major: No); Sex Chromosomes (UI: D012730, Major: No); Skin Abnormalities (UI: D012868, Major: No) | Aortic Diseases|Bone and Bones|Brain Diseases|Collagen|Connective Tissue|Cutis Laxa|Ehlers-Danlos Syndrome|Fascia|Genetic Linkage|Homocystinuria|Humans|Hydroxylysine|Hydroxyproline|Joints|Marfan Syndrome|Microbial Collagenase|Osteogenesis Imperfecta|Protein Biosynthesis|Protein Conformation|Protein-Lysine 6-Oxidase|Sex Chromosomes|Skin Abnormalities | etiology (0)|abnormalities (0)|genetics (0)|biosynthesis (1); metabolism (0)|metabolism (1)|metabolism (0); pathology (0)|genetics (0); metabolism (0); pathology (0)|abnormalities (0)||metabolism (0)||biosynthesis (0)|biosynthesis (0); urine (0)|abnormalities (0)|metabolism (0)|metabolism (0)|metabolism (0); pathology (0)|||deficiency (0)|| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-01 | 2019-07-23 | pubmed: 1976-2-1; medline: 1976-2-1 0:1; entrez: 1976-2-1 0:0 | pubmed: 1448; pii: S0022-202X(15)44682-2; doi: 10.1111/1523-1747.ep12481404 | Heart Defects, Congenital | ['Marfan Syndrome'] |
1,567 | 1 | [Certain problems of treatment of ischemic heart disease]. | MEDLINE | Manual | NLM | On the basis of extended personal experience and of the literature data, the authors give recommendations for differentiated rational drug therapy of different stages of ischaemic heart disease. The results of a study of comparative efficacy of 15 coronary-active drugs used in 709 patients with ischaemic heart disease are presented along with their clinical pharmacology, side effects, indications and counterindications. The conclusions were arrived at on the basis of an objective clinical and laboratory study of the effect of the drugs. The methods of evaluation of the drug's efficacy and of the selection of patients for the administration of adequate therapy are described, which permits to use these recommendations for practical purposes. Some problems of the pathogenesis of ischaemic heart disease are discussed in terms of the selection of pathogenetic therapy. | Kardiologiia | 0022-9040 | Print | 15 | 7 | Print | 1,975 | Jul | null | 16-24 | I P Zamotaev (IP); L G Lozinskiĭ (LG); M G Venediktova (MG); B L Sandomirskiĭ (BL) | English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Vasodilator Agents (Registry: 0, UI: D014665) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); physiopathology (UI: Q000503, Major: No); Drug Evaluation (UI: D004341, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Humans (UI: D006801, Major: No); Myocardial Contraction (UI: D009200, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Vasodilator Agents (UI: D014665, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: No) | Adrenergic beta-Antagonists|Angina Pectoris|Coronary Disease|Drug Evaluation|Heart|Humans|Myocardial Contraction|Vasodilator Agents | pharmacology (0); therapeutic use (1)|drug therapy (0)|drug therapy (1); physiopathology (0)||physiopathology (0)||drug effects (0)|pharmacology (0); therapeutic use (0) | 0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2017-03-10 | pubmed: 1975-7-1; medline: 1975-7-1 0:1; entrez: 1975-7-1 0:0 | pubmed: 1567 | Myocardial Ischemia | ['Angina Pectoris', 'Coronary Disease'] |
1,568 | 1 | [Stimulators of beta-adrenergic structures in treatment of ischemic heart disease]. | MEDLINE | Manual | NLM | The beneficial effect of stimulators of beta-adrenergic structures (Myophedrin on the haemodynamics and the inotropic function of the myocardium was demonstrated experimentally (in 12 rabbits) and clinically (in 53 patients with ischaemic heart disease). A positive effect of the treatment was noted in 45.5% of those patients in whom ischaemic heart disease manifested itself in angina decubitus and angina of effort. | Kardiologiia | 0022-9040 | Print | 15 | 7 | Print | 1,975 | Jul | null | 37-43 | F I Komarov (FI); L I Ol'binskaia (LI); A A Abinder (AA); V V Iankin (VV); I T Kitaeva (IT) | English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Agonists (Registry: 0, UI: D000318) | Adrenergic beta-Agonists (UI: D000318, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes); Adult (UI: D000328, Major: No); Aged (UI: D000368, Major: No); Animals (UI: D000818, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); physiopathology (UI: Q000503, Major: No); Electrocardiography (UI: D004562, Major: No); Female (UI: D005260, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Hemodynamics (UI: D006439, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Myocardial Contraction (UI: D009200, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: Yes); Rabbits (UI: D011817, Major: No); Stimulation, Chemical (UI: D013268, Major: No) | Adrenergic beta-Agonists|Adult|Aged|Animals|Coronary Disease|Electrocardiography|Female|Heart|Hemodynamics|Humans|Male|Middle Aged|Myocardial Contraction|Rabbits|Stimulation, Chemical | pharmacology (0); therapeutic use (1)||||drug therapy (1); physiopathology (0)|||physiopathology (0)|drug effects (0)||||drug effects (1)|| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2017-03-10 | pubmed: 1975-7-1; medline: 1975-7-1 0:1; entrez: 1975-7-1 0:0 | pubmed: 1568 | Myocardial Ischemia | ['Coronary Disease'] |
1,569 | 1 | [Nonachlasine--a new drug for treatment of ischemic heart disease]. | MEDLINE | Manual | NLM | Data on the pharmacology of a new antianginal drug--Nonachlasine--are presented. Nonachlasine was found to increase the blood flow intensively and for long periods of time, increasing the oxygen reserve of the myocardium, thus increasing the cardiac output and the contractile function of the heart. The prevailing action of Nonachlasine on the blood supply and the function of the myocardium seems to be the result of several mechanisms: decreasing resistance of the coronaries due to the activation of the beta2-adrenergic structures; influence upon the extravascular factors of the regulation of the coronary circulation (changes in the metabolism and cardiac activity due to the excitation of the beta-adrenergic structures). The mechanism of the positive effect of Nonachlasine upon the blood supply and function of the heart is connected with its action on the adrenergic processes. The drug accumulates noradrenaline in the myocardium and increases the activity of phosphorilase-a. This coincides in time with the increased blood supply and contractile capacity of the heart. The beta-adrenoblocking agents prevent these effects. It was postulated that the effect of Nonachlasine in the blood supply and the activity of the heart is connected with its ability to utilize the energy reserve of the myocardium by way of switching over to the anaerobic way. | Kardiologiia | 0022-9040 | Print | 15 | 7 | Print | 1,975 | Jul | null | 43-8 | N V Kaverina (NV); G A Markova (GA); G G Chichkanov (GG); V B Chumburidze (VB); A I Basaeva (AI) | English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Agonists (Registry: 0, UI: D000318); Phenothiazines (Registry: 0, UI: D010640) | Adrenergic beta-Agonists (UI: D000318, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes); Animals (UI: D000818, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Cardiac Output (UI: D002302, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Cats (UI: D002415, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); physiopathology (UI: Q000503, Major: No); Drug Evaluation (UI: D004341, Major: No); Hemodynamics (UI: D006439, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Phenothiazines (UI: D010640, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes); Rabbits (UI: D011817, Major: No); Rats (UI: D051381, Major: No); Regional Blood Flow (UI: D012039, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Vascular Resistance (UI: D014655, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No) | Adrenergic beta-Agonists|Animals|Blood Pressure|Cardiac Output|Cats|Coronary Disease|Drug Evaluation|Hemodynamics|Phenothiazines|Rabbits|Rats|Regional Blood Flow|Vascular Resistance | therapeutic use (1)||drug effects (0)|drug effects (0)||drug therapy (1); physiopathology (0)||drug effects (0)|therapeutic use (1)|||drug effects (0)|drug effects (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2017-03-10 | pubmed: 1975-7-1; medline: 1975-7-1 0:1; entrez: 1975-7-1 0:0 | pubmed: 1569 | Myocardial Ischemia | ['Coronary Disease'] |
1,570 | 1 | [Cordaron and nonachlasine in treatment of chronic coronary insufficiency]. | MEDLINE | Manual | NLM | In a double blind study of the clinical effect of Cordaron conducted in 55 patients with chronic ischaemic heart disease a positive effect was obtained in 80.4% of the cases, an effect of placebo-in 24.3%. Cordaron was especially effective in patients with localized stenoses of the coronary arteries. Nonachlasine (an activator of the cardiac beta-adrenergic receptors) proved effective in 10 of 13 patients with chronic ischaemic heart disease. | Kardiologiia | 0022-9040 | Print | 15 | 7 | Print | 1,975 | Jul | null | 48-51 | V I Metelitsa (VI); L S Matveeva (LS); G A Borisova (GA); V P Lupanov (VP) | Clinical Trial (D016430); Controlled Clinical Trial (D018848); English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Agonists (Registry: 0, UI: D000318); Benzofurans (Registry: 0, UI: D001572); Phenothiazines (Registry: 0, UI: D010640); Amiodarone (Registry: N3RQ532IUT, UI: D000638) | Adrenergic beta-Agonists (UI: D000318, Major: No) - Qualifiers: administration & dosage (UI: Q000008, Major: No); therapeutic use (UI: Q000627, Major: Yes); Amiodarone (UI: D000638, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes); Benzofurans (UI: D001572, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes); Chronic Disease (UI: D002908, Major: No); Clinical Trials as Topic (UI: D002986, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); Drug Evaluation (UI: D004341, Major: No); Follow-Up Studies (UI: D005500, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Phenothiazines (UI: D010640, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes) | Adrenergic beta-Agonists|Amiodarone|Benzofurans|Chronic Disease|Clinical Trials as Topic|Coronary Disease|Drug Evaluation|Follow-Up Studies|Humans|Male|Middle Aged|Phenothiazines | administration & dosage (0); therapeutic use (1)|therapeutic use (1)|therapeutic use (1)|||drug therapy (1)||||||therapeutic use (1) | 0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2017-03-10 | pubmed: 1975-7-1; medline: 1975-7-1 0:1; entrez: 1975-7-1 0:0 | pubmed: 1570 | Myocardial Ischemia | ['Coronary Disease'] |
1,571 | 1 | [Effect of certain drugs, used in treatment of chronic coronary insufficiency, on adenosine metabolism]. | MEDLINE | Manual | NLM | It has been demonstrated that the study of the activity of 5'-nucleotidase and adenosine-desaminase permits to interpret the metabolism of adenosine. Curanthil, Sustac and Intensain influence the adenosine metabolism favouring an elevation of its content. The therapeutic effect of Obsidan is not conditioned by the ""adenosine"" metabolism. | Kardiologiia | 0022-9040 | Print | 15 | 7 | Print | 1,975 | Jul | null | 51-6 | E Sh Khalfen (ESh); S G Denisova (SG) | English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Vasodilator Agents (Registry: 0, UI: D014665); Nucleotidases (Registry: EC 3.1.3.-, UI: D009708); Adenosine Deaminase (Registry: EC 3.5.4.4, UI: D000243); Adenosine (Registry: K72T3FS567, UI: D000241) | Adenosine (UI: D000241, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Adenosine Deaminase (UI: D000243, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes); Adult (UI: D000328, Major: No); Aged (UI: D000368, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); enzymology (UI: Q000201, Major: No); metabolism (UI: Q000378, Major: No); Female (UI: D005260, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: enzymology (UI: Q000201, Major: No); Nucleotidases (UI: D009708, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Vasodilator Agents (UI: D014665, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes) | Adenosine|Adenosine Deaminase|Adrenergic beta-Antagonists|Adult|Aged|Coronary Disease|Female|Humans|Male|Middle Aged|Myocardium|Nucleotidases|Vasodilator Agents | metabolism (1)|metabolism (0)|therapeutic use (1)|||drug therapy (1); enzymology (0); metabolism (0)|||||enzymology (0)|metabolism (0)|therapeutic use (1) | 0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2017-03-10 | pubmed: 1975-7-1; medline: 1975-7-1 0:1; entrez: 1975-7-1 0:0 | pubmed: 1571 | Myocardial Ischemia | ['Coronary Disease'] |
1,704 | 1 | Cardiovascular effects of electrical stimulation of the forebrain in the fetal lamb. | MEDLINE | Manual | NLM | Modified stereotaxic techniques were applied to fetal lambs during the latter third of gestation. Electrical stimulation in the region of the hypothalamus in 10 acute experiments was associated with three patterns of arterial blood pressure and heart rate changes: a pressor-tachycardia response; a pure tachycardia response (abolished by propranolol); and a pure bradycardia response (abolished by atropine). The pressor-tachycardia response was examined in detail in 13 chronic preparations (115-135 days of gestation at operation). The systolic arterial blood pressure increase was never greater than 35 mm Hg and was probably blunted by the large noninnervated placental circulation. This pressure increase was abolished by phentolamine and was thus mediated by stimulation of alpha-adrenergic receptors. The initial tachycardia was prevented by propranolol and was due to beta-adrenergic stimulation. The tachycardia was followed in a few seconds by a bradycardia, abolished by atropine and possibly a vagal baroreflex. The pressor-tachycardia response was accentuated in two lambs who were delivered spontaneously and were studied after birth. These studies indicate that a suprabulbar neural framework exists in the fetal lamb for influencing the cardiovascular system from as early as 90 days of gestation. | Pediatric research | 0031-3998 | Print | 10 | 1 | Print | 1,976 | Jan | null | 40-5 | R L Williams (RL); R P Hof (RP); M A Heymann (MA); A M Rudolph (AM) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Animals (UI: D000818, Major: No); Blood Pressure (UI: D001794, Major: Yes) - Qualifiers: drug effects (UI: Q000187, Major: No); Bradycardia (UI: D001919, Major: No) - Qualifiers: etiology (UI: Q000209, Major: No); Electric Stimulation (UI: D004558, Major: No); Heart Rate (UI: D006339, Major: Yes) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Hypothalamus (UI: D007031, Major: No) - Qualifiers: embryology (UI: Q000196, Major: No); physiology (UI: Q000502, Major: Yes); Sheep (UI: D012756, Major: No); Stereotaxic Techniques (UI: D013238, Major: No); Tachycardia (UI: D013610, Major: No) - Qualifiers: etiology (UI: Q000209, Major: No) | Adrenergic beta-Antagonists|Animals|Blood Pressure|Bradycardia|Electric Stimulation|Heart Rate|Humans|Hypothalamus|Sheep|Stereotaxic Techniques|Tachycardia | pharmacology (0)||drug effects (0)|etiology (0)||drug effects (0)||embryology (0); physiology (1)|||etiology (0) | 0|0|1|0|0|1|0|0|0|0|0 | null | 1976-03-30 | 2006-11-15 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 1704; doi: 10.1203/00006450-197601000-00008 | Arrhythmias, Cardiac | ['Bradycardia', 'Tachycardia'] |
1,832 | 1 | Effects of pH and pCO2 on performance of ischemic myocardium. | MEDLINE | Manual | NLM | Contractile performance of ischemic feline myocardium was evaluated under conditions of selective changes in perfusate in pH and pCO2. A substantial increase in myocardial performance was noted when the pCO2 was lowered at constant pH, and depression of performance was noted when the pCO2 was increased at constant pH. Perfusate acidosis at constant pCO2 resulted in depression of performance and decreased performance only after 20 min of exposure. Alkalosis did not increase performance and decreased performance transiently during mild ischemia. These studies suggest that performance of myocardium during ischemia is closely related to tissue pCO2 and is minimally related to the level of extracellular pH. | Recent advances in studies on cardiac structure and metabolism | 0363-5872 | Print | 10 | null | Print | 1,975 | null | null | 355-64 | M L Weisfeldt (ML); R L Bishop (RL); H L Greene (HL) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Carbon Dioxide (Registry: 142M471B3J, UI: D002245) | Acidosis (UI: D000138, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); physiopathology (UI: Q000503, Major: No); Alkalosis (UI: D000471, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); physiopathology (UI: Q000503, Major: No); Animals (UI: D000818, Major: No); Carbon Dioxide (UI: D002245, Major: No) - Qualifiers: blood (UI: Q000097, Major: Yes); Cats (UI: D002415, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); physiopathology (UI: Q000503, Major: Yes); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: Yes); Hydrogen-Ion Concentration (UI: D006863, Major: Yes); Pressure (UI: D011312, Major: No) | Acidosis|Alkalosis|Animals|Carbon Dioxide|Cats|Coronary Disease|Heart|Hydrogen-Ion Concentration|Pressure | metabolism (0); physiopathology (0)|metabolism (0); physiopathology (0)||blood (1)||metabolism (0); physiopathology (1)|physiopathology (1)|| | 0|0|0|0|0|0|0|1|0 | null | 1976-04-01 | 2013-11-21 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 1832 | Myocardial Ischemia | ['Coronary Disease'] |
1,849 | 1 | Roentgenological findings in cryptorchidism. | MEDLINE | Manual | NLM | Intravenous urography of 78 cryptorchid boys revealed no clinically significant upper urinary tract anomalies. Two boys had a rotated kidney and 2 others a double renal pelvis. One boy had previously been operated upon because of hydronephrosis. There thus appears to be no reason for routine intravenous urography of cryptorchid boys. Forty-two per cent of the boys had spina bifida occulta in the lumbar and sacral spine. One case of asymptomatic congenital cardiac disease was discovered at routine chest X-ray. | Scandinavian journal of urology and nephrology | 0036-5599 | Print | 9 | 3 | Print | 1,975 | null | null | 171-3 | K J Tveter (KJ); J Fjaerli (J) | Journal Article (D016428) | null | Abnormalities, Multiple (UI: D000015, Major: No); Cryptorchidism (UI: D003456, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); diagnostic imaging (UI: Q000000981, Major: Yes); Heart Defects, Congenital (UI: D006330, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Humans (UI: D006801, Major: No); Kidney (UI: D007668, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: No); Male (UI: D008297, Major: No); Spinal Dysraphism (UI: D016135, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Urography (UI: D014567, Major: No) | Abnormalities, Multiple|Cryptorchidism|Heart Defects, Congenital|Humans|Kidney|Male|Spinal Dysraphism|Urography | |complications (0); diagnostic imaging (1)|complications (0)||abnormalities (0)||complications (0)| | 0|0|0|0|0|0|0|0 | null | 1976-03-18 | 2019-09-02 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 1849; doi: 10.3109/00365597509134205 | Heart Defects, Congenital | [] |
1,865 | 1 | Direct revascularization of acute myocardial infarction by implantation of left internal mammary artery into infarcted left ventricular myocardium. | MEDLINE | Manual | NLM | This is a preliminary report. Clearly, the internal mammary artery implanted into the infarcted anterolateral portion of the wall of the left ventricle has been of help in decreasing the size of the infarction and in maintaining the life of the dogs and normal function six hours after a large left ventricular wall myocardial infarction had been created. More animals need to be studied at the end of six hours, eight hours, and ten hours after implantation. More studies are needed to learn if ligation of the coronary veins at the same time as the arteries is beneficial or not. Two internal mammary arteries may act better than one when implanted side by side into a 5 by 5 centimeter infarction. In man, both internal mammary arteries and the right gastroepiploic artery could be used to revascularize acute myocardial infarctions in the posterior and anterolateral parts of the left ventricle. | Surgery, gynecology & obstetrics | 0039-6087 | Print | 140 | 1 | Print | 1,975 | Jan | null | 44-52 | A Vineberg (A); S Afridi (S); S Sahi (S) | Journal Article (D016428) | null | Acute Disease (UI: D000208, Major: No); Animals (UI: D000818, Major: No); Coronary Artery Bypass (UI: D001026, Major: No) - Qualifiers: methods (UI: Q000379, Major: No); Dogs (UI: D004285, Major: No); Humans (UI: D006801, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); pathology (UI: Q000473, Major: No); surgery (UI: Q000601, Major: Yes); Myocardial Revascularization (UI: D009204, Major: Yes) - Qualifiers: methods (UI: Q000379, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No); Radiography (UI: D011859, Major: No) | Acute Disease|Animals|Coronary Artery Bypass|Dogs|Humans|Myocardial Infarction|Myocardial Revascularization|Myocardium|Radiography | ||methods (0)|||diagnostic imaging (0); pathology (0); surgery (1)|methods (0)|pathology (0)| | 0|0|0|0|0|0|1|0|0 | null | 1976-04-01 | 2016-11-23 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 1865 | Myocardial Ischemia | ['Myocardial Infarction'] |
1,868 | 1 | Effects of beta-adrenergic stimulating and blocking agents on the adrenaline response and adenyl cyclase activity of leukocyte in monkey and human being. | MEDLINE | Manual | NLM | Using the method in which leukocyte suspensions were incubated with NaF or metaproterenol at 30 degrees C for 15-30 min to allow them to convert 3H-ATP (10 muCi) to 3H-cyclic AMP, followed by separation of the formed 3H-cyclic AMP by common chromatography, the leukocyte adenyl cyclase activity of monkeys and human beings was measured with high reproducibility. The oral administration of metaproterenol increased the leukocyte adenyl cyclase activity which was stimulated by NaF and decreased the count of peripheral eosinophils in some of the monkeys. In the beta-adrenergic blockade of the monkey which was made by administration of propranolol, the leukocyte adenyl cyclase activity significantly decreased. The leukocyte adenyl cyclase from patients with coronary heart disease also decreased after oral medication with propranolol. | The Tohoku journal of experimental medicine | 0040-8727 | Print | 117 | 2 | Print | 1,975 | Oct | null | 125-33 | S Mue (S); T Ise (T); K Akasaka (K); T Takishima (T) | Journal Article (D016428) | Adrenergic beta-Agonists (Registry: 0, UI: D000318); Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Blood Glucose (Registry: 0, UI: D001786); Lactates (Registry: 0, UI: D007773); Metaproterenol (Registry: 53QOG569E0, UI: D009921); Propranolol (Registry: 9Y8NXQ24VQ, UI: D011433); Adenylyl Cyclases (Registry: EC 4.6.1.1, UI: D000262); Epinephrine (Registry: YKH834O4BH, UI: D004837) | Adenylyl Cyclases (UI: D000262, Major: No) - Qualifiers: blood (UI: Q000097, Major: Yes); Adrenergic beta-Agonists (UI: D000318, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Aged (UI: D000368, Major: No); Animals (UI: D000818, Major: No); Blood Glucose (UI: D001786, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: enzymology (UI: Q000201, Major: No); Eosinophils (UI: D004804, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Epinephrine (UI: D004837, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); pharmacology (UI: Q000494, Major: Yes); Female (UI: D005260, Major: No); Haplorhini (UI: D000882, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Lactates (UI: D007773, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Leukocytes (UI: D007962, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); enzymology (UI: Q000201, Major: Yes); Male (UI: D008297, Major: No); Metaproterenol (UI: D009921, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Middle Aged (UI: D008875, Major: No); Propranolol (UI: D011433, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Time Factors (UI: D013997, Major: No) | Adenylyl Cyclases|Adrenergic beta-Agonists|Adrenergic beta-Antagonists|Aged|Animals|Blood Glucose|Coronary Disease|Eosinophils|Epinephrine|Female|Haplorhini|Heart Rate|Humans|Lactates|Leukocytes|Male|Metaproterenol|Middle Aged|Propranolol|Time Factors | blood (1)|pharmacology (1)|pharmacology (1)|||metabolism (0)|enzymology (0)|drug effects (0)|blood (0); pharmacology (1)|||drug effects (0)||blood (0)|drug effects (0); enzymology (1)||pharmacology (0)||pharmacology (0)| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-03-30 | 2019-07-27 | pubmed: 1975-10-1; medline: 1975-10-1 0:1; entrez: 1975-10-1 0:0 | pubmed: 1868; doi: 10.1620/tjem.117.125 | Myocardial Ischemia | ['Coronary Disease'] |
2,004 | 1 | Electrocardiographic changes and cardiac arrhythmias in patients receiving psychotropic drugs. | MEDLINE | Manual | NLM | Eight patients had cardiac manifestations that were life-threatening in five while taking psychotropic drugs, either phenothiazines or tricyclic antidepressants. Although most patients were receiving several drugs, Mellaril (thioridazine) appeared to be responsible for five cases of ventricular tachycardia, one of which was fatal in a 35 year old woman. Supraventricular tachycardia developed in one patient receiving Thorazine (chlorpromazine). Aventyl (nortriptyline) and Elavil (amitriptyline) each produced left bundle branch block in a 73 year old woman. Electrocardiographic T and U wave abnormalities were present in most patients. The ventricular arrhythmias responded to intravenous administration of lidocaine and to direct current electric shock; ventricular pacing was required in some instances and intravenous administration of propranolol combined with ventricular pacing in one. The tachyarrhythmias generally subsided within 48 hours after administration of the drugs was stopped. Five of the eight patients were 50 years of age or younger; only one clearly had antecedent heart disease. Major cardiac arrhythmias are a potential hazard in patients without heart disease who are receiving customary therapeutic doses of psychotropic drugs. A prospective clinical trial is suggested to quantify the risk of cardiac complications to patients receiving phenothiazines or tricyclic antidepressant drugs. | The American journal of cardiology | 0002-9149 | Print | 37 | 2 | Print | 1,976 | Feb | null | 223-30 | N O Fowler (NO); D McCall (D); T C Chou (TC); J C Holmes (JC); I B Hanenson (IB) | Case Reports (D002363); Journal Article (D016428) | Adrenergic Agonists (Registry: 0, UI: D000322); Antidepressive Agents, Tricyclic (Registry: 0, UI: D000929); Digitalis Glycosides (Registry: 0, UI: D004071); Diuretics (Registry: 0, UI: D004232); Phenothiazines (Registry: 0, UI: D010640); Psychotropic Drugs (Registry: 0, UI: D011619); Mesoridazine (Registry: 5XE4NWM740, UI: D008653); Lidocaine (Registry: 98PI200987, UI: D008012); Thioridazine (Registry: N3D6TG58NI, UI: D013881); Chlorpromazine (Registry: U42B7VYA4P, UI: D002746) | Adrenergic Agonists (UI: D000322, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Adult (UI: D000328, Major: No); Aged (UI: D000368, Major: No); Antidepressive Agents, Tricyclic (UI: D000929, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Arrhythmias, Cardiac (UI: D001145, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: Yes); drug therapy (UI: Q000188, Major: No); Cardiovascular System (UI: D002319, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Chlorpromazine (UI: D002746, Major: No) - Qualifiers: adverse effects (UI: Q000009, Major: No); Digitalis Glycosides (UI: D004071, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Diuretics (UI: D004232, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Electrocardiography (UI: D004562, Major: Yes); Female (UI: D005260, Major: No); Heart Failure (UI: D006333, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); drug therapy (UI: Q000188, Major: No); Humans (UI: D006801, Major: No); Hypotension (UI: D007022, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); drug therapy (UI: Q000188, Major: No); Lidocaine (UI: D008012, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Male (UI: D008297, Major: No); Mesoridazine (UI: D008653, Major: No) - Qualifiers: adverse effects (UI: Q000009, Major: No); Middle Aged (UI: D008875, Major: No); Phenothiazines (UI: D010640, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Psychotropic Drugs (UI: D011619, Major: No) - Qualifiers: adverse effects (UI: Q000009, Major: Yes); Thioridazine (UI: D013881, Major: No) - Qualifiers: adverse effects (UI: Q000009, Major: No) | Adrenergic Agonists|Adult|Aged|Antidepressive Agents, Tricyclic|Arrhythmias, Cardiac|Cardiovascular System|Chlorpromazine|Digitalis Glycosides|Diuretics|Electrocardiography|Female|Heart Failure|Humans|Hypotension|Lidocaine|Male|Mesoridazine|Middle Aged|Phenothiazines|Psychotropic Drugs|Thioridazine | therapeutic use (0)|||pharmacology (0)|chemically induced (1); drug therapy (0)|drug effects (0)|adverse effects (0)|therapeutic use (0)|therapeutic use (0)|||chemically induced (0); drug therapy (0)||chemically induced (0); drug therapy (0)|therapeutic use (0)||adverse effects (0)||pharmacology (0)|adverse effects (1)|adverse effects (0) | 0|0|0|0|0|0|0|0|0|1|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2019-06-22 | pubmed: 1976-2-1; medline: 1976-2-1 0:1; entrez: 1976-2-1 0:0 | pubmed: 2004; pii: 0002-9149(76)90316-7; doi: 10.1016/0002-9149(76)90316-7 | Heart Failure | [] |
2,074 | 1 | [Congenital cardiopathies appearing during the neonatal period. The view points of the cardiologist, the hemodynamics specialist, the surgeon, and the anesthetist]. | MEDLINE | Manual | NLM | The best chances of survival for a new-born depend on the following factors: the possibility of clinical and haemodynamic diagnosis of the malformation, adequate reanimation and surgery. All this must be carried out as early as possible. Although catheterization is very risky it should be complete and as fast as possible, under monitoring of ventilation and haemodynamies. Reanimation is very important before, during and after surgery; it should be more preventive than curative. Very often, surgery is only palliative at this age. Taking into account progress in surgical techniques, the authors report their experience in anaesthesia and ressuscitation of 100 patients under 10 days old. They were all operated on in Laennec in Professor MATHEY's department but only some of them were catheterized there. | Annales de l'anesthesiologie francaise | 0003-4061 | Print | 16 Spec No 1 | null | Print | 1,975 | null | null | 161-9 | A Fiemeyer (A); F Leca-Chetochine (F); M Thibert (M); Y Louville (Y); J Mathey (J); M Cara (M) | English Abstract (D004740); Journal Article (D016428) | null | Anesthesia, General (UI: D000768, Major: Yes); Aortic Coarctation (UI: D001017, Major: No) - Qualifiers: surgery (UI: Q000601, Major: No); Cardiac Catheterization (UI: D006328, Major: No); Heart Defects, Congenital (UI: D006330, Major: No) - Qualifiers: surgery (UI: Q000601, Major: Yes); Humans (UI: D006801, Major: No); Infant, Newborn (UI: D007231, Major: No); Preoperative Care (UI: D011300, Major: No); Tetralogy of Fallot (UI: D013771, Major: No) - Qualifiers: surgery (UI: Q000601, Major: No); Transposition of Great Vessels (UI: D014188, Major: No) - Qualifiers: surgery (UI: Q000601, Major: No) | Anesthesia, General|Aortic Coarctation|Cardiac Catheterization|Heart Defects, Congenital|Humans|Infant, Newborn|Preoperative Care|Tetralogy of Fallot|Transposition of Great Vessels | |surgery (0)||surgery (1)||||surgery (0)|surgery (0) | 1|0|0|0|0|0|0|0|0 | null | 1976-03-30 | 2017-03-22 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 2074 | Heart Defects, Congenital | ['Aortic Coarctation', 'Tetralogy of Fallot', 'Transposition of Great Vessels'] |
2,092 | 1 | Effects of the cardioselective beta-blocker metoprolol in angina pectoris. A subacute study with exercise tests. | MEDLINE | Manual | NLM | The effects of the cardioselective beta-blocker, metoprolol, were evaluated under double-blind conditions in eighteen patients with angina pectoris. During an introductory run-in period of eight weeks, a placebo was given single-blindly. Thereafter two double-blind crossover periods each of four weeks followed, either 20 mg metroprolol or placebo being given t.i.d. Metoprolol gave a significant reduction in the number of anginal attacks and in nitroglycerin consumption. The patients' subjective assessments of their daily angina pectoris symptoms also showed a significant improvement compared with the placebo. At the end of each period, a standardized exercise test was performed. In comparison with placebo, metoprolol gave a significant increase of total work performed until the appearance of 1 mm ST-segment depression and until the end of exercise. The heart rate was significantly reduced at rest and during exercise. The blood pressure was significantly reduced only during exercise. None of the patients reported any severe unwanted effects. The complaints reported were mild to moderate, and the frequency during metoprolol treatment was even lower than during placebo treatment. No signs or symptoms of cardiac failure were seen in any of these patients on any occasion. It is concluded that 20 mg metoprolol t.i.d. is of benefit in the treatment of angina pectoris but further benefit might be obtained with higher doses. | Annals of clinical research | 0003-4762 | Print | 7 | 6 | Print | 1,975 | Dec | null | 433-41 | O Keyriläinen (O); A Uustialo (A) | Clinical Trial (D016430); Controlled Clinical Trial (D018848); Journal Article (D016428); Randomized Controlled Trial (D016449) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Propanolamines (Registry: 0, UI: D011412) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: adverse effects (UI: Q000009, Major: No); therapeutic use (UI: Q000627, Major: Yes); Adult (UI: D000328, Major: No); Aged (UI: D000368, Major: No); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Cardiac Output (UI: D002302, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Clinical Trials as Topic (UI: D002986, Major: No); Drug Evaluation (UI: D004341, Major: No); Exercise Test (UI: D005080, Major: No); Female (UI: D005260, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); In Vitro Techniques (UI: D066298, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: adverse effects (UI: Q000009, Major: No); therapeutic use (UI: Q000627, Major: Yes); Time Factors (UI: D013997, Major: No) | Adrenergic beta-Antagonists|Adult|Aged|Angina Pectoris|Blood Pressure|Cardiac Output|Clinical Trials as Topic|Drug Evaluation|Exercise Test|Female|Heart Rate|Humans|In Vitro Techniques|Male|Middle Aged|Propanolamines|Time Factors | adverse effects (0); therapeutic use (1)|||drug therapy (1)|drug effects (0)|drug effects (0)|||||drug effects (0)|||||adverse effects (0); therapeutic use (1)| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-02 | 2014-11-20 | pubmed: 1975-12-1; medline: 1975-12-1 0:1; entrez: 1975-12-1 0:0 | pubmed: 2092 | Myocardial Ischemia | ['Angina Pectoris'] |
2,481 | 1 | Cardiovascular and beta-adrenergic blocking effects of timolol. | MEDLINE | Manual | NLM | The haemodynamic effects of timolol and its inhibiting action on the cardiovascular and bronchial effects of isoproterenol have been studied. Splanchnic nerve activity was recorded. The antiarrhythmic action of timolol was studied on guinea pig isolated atria, using arrhythmias induced by epinephrine, ouabain or coronary ligation in the dog. Timolol is a very potent beta-adrenoceptor blocking agent, without specificity on beta1- or beta2-receptors. No intrinsic beta-stimulating or depressant effects were found. Timolol reduced splanchnic discharges. The antiarrhythmic effect of timolol was limited to epinephrine-induced arrhythmias. | European journal of pharmacology | 0014-2999 | Print | 35 | 2 | Print | 1,976 | Feb | null | 235-43 | P Mouillé (P); H Schmitt (H); G Cheymol (G); E Gauter (E) | Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Propanolamines (Registry: 0, UI: D011412); Thiadiazoles (Registry: 0, UI: D013830); Propranolol (Registry: 9Y8NXQ24VQ, UI: D011433); Isoproterenol (Registry: L628TT009W, UI: D007545) | Adrenergic beta-Antagonists (UI: D000319, Major: Yes); Airway Resistance (UI: D000403, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Animals (UI: D000818, Major: No); Aorta (UI: D001011, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Arrhythmias, Cardiac (UI: D001145, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); physiopathology (UI: Q000503, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Bronchi (UI: D001980, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Coronary Circulation (UI: D003326, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Dogs (UI: D004285, Major: No); Female (UI: D005260, Major: No); Guinea Pigs (UI: D006168, Major: No); Heart Atria (UI: D006325, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Hemodynamics (UI: D006439, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: Yes); In Vitro Techniques (UI: D066298, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); Male (UI: D008297, Major: No); Myocardial Contraction (UI: D009200, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Propranolol (UI: D011433, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Splanchnic Nerves (UI: D013153, Major: No) - Qualifiers: physiology (UI: Q000502, Major: No); Thiadiazoles (UI: D013830, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Time Factors (UI: D013997, Major: No) | Adrenergic beta-Antagonists|Airway Resistance|Animals|Aorta|Arrhythmias, Cardiac|Blood Pressure|Bronchi|Coronary Circulation|Dogs|Female|Guinea Pigs|Heart Atria|Heart Rate|Hemodynamics|In Vitro Techniques|Isoproterenol|Male|Myocardial Contraction|Propanolamines|Propranolol|Splanchnic Nerves|Thiadiazoles|Time Factors | |drug effects (0)||drug effects (0)|chemically induced (0); physiopathology (0)|drug effects (0)|drug effects (0)|drug effects (0)||||drug effects (0)|drug effects (0)|drug effects (1)||antagonists & inhibitors (0)||drug effects (0)|pharmacology (1)|pharmacology (0)|physiology (0)|pharmacology (1)| | 1|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-19 | 2019-06-23 | pubmed: 1976-2-1; medline: 1976-2-1 0:1; entrez: 1976-2-1 0:0 | pubmed: 2481; pii: 0014-2999(76)90225-9; doi: 10.1016/0014-2999(76)90225-9 | Arrhythmias, Cardiac | [] |
2,527 | 1 | [Inflammatory cerebro-vascular disease: angiographic findings and distribution patterns (author's transl)]. | MEDLINE | Manual | NLM | Although cerebral angiography should be approached with caution in the diagnosis of inflammatory cerebro-vascular disease there are some characteristic angiographic findings which may be helpful for classification and differential diagnosis. The proximal cerebral arteries are favourably affected by basal meningitis and thrombangiitis obliterans with resulting stenoses and occlusions. Whereas those inflammations originating from neighbouring skull structures mostly involve the intracavernous parts of the carotid artery, the tuberculous and mycotic arteritis prefer the supraclinoid carotid siphon. Peripheral vascular changes are found in luetic endangiitis, necrotizing and toxic angiitis and in collagenoses. Simultaneous involvement of the temporal arteries is of great diagnostic importance demonstrating the systemic character of the inflammatory process; in Horton's arteritis it can be a pathognomonic finding. Infectious endocarditis, some mycoses and malaria may lead to embolic occlusion of cerebral vessels. Mycotic aneurysms mostly have a broad base or a fusiform shape and do not prefer the localizations of congenital aneurysms. Angiographically, abscesses, tuberculomas and viral encephalitis may result in circumscribed hypervascularized areas. The characteristic angiographic findings are exemplified and discussed on the basis of 8 cases of inflammatory cerebro-vascular disease (tuberculosis, pneumococcal and unspecific bacterial meningitis, syphilis, mycosis, Takayasu-syndrome, panarteritis nodosa, temporal arteritis). | Fortschritte der Neurologie, Psychiatrie, und ihrer Grenzgebiete | 0015-8194 | Print | 43 | 12 | Print | 1,975 | Dec | null | 631-47 | P Stoeter (P); E Ortega-Suhrkamp (E); K Voigt (K) | Journal Article (D016428) | null | Adult (UI: D000328, Major: No); Arteritis (UI: D001167, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); Cerebral Angiography (UI: D002533, Major: No); Cerebrovascular Disorders (UI: D002561, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); diagnostic imaging (UI: Q000000981, Major: Yes); Diagnosis, Differential (UI: D003937, Major: No); Female (UI: D005260, Major: No); Giant Cell Arteritis (UI: D013700, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); Humans (UI: D006801, Major: No); Malaria (UI: D008288, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); Male (UI: D008297, Major: No); Meningitis (UI: D008581, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Middle Aged (UI: D008875, Major: No); Mycoses (UI: D009181, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); Polyarteritis Nodosa (UI: D010488, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); Syphilis, Cardiovascular (UI: D013589, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No); Thromboangiitis Obliterans (UI: D013919, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Tuberculosis, Cardiovascular (UI: D014381, Major: No) - Qualifiers: diagnostic imaging (UI: Q000000981, Major: No) | Adult|Arteritis|Cerebral Angiography|Cerebrovascular Disorders|Diagnosis, Differential|Female|Giant Cell Arteritis|Humans|Malaria|Male|Meningitis|Middle Aged|Mycoses|Polyarteritis Nodosa|Syphilis, Cardiovascular|Thromboangiitis Obliterans|Tuberculosis, Cardiovascular | |diagnostic imaging (0)||complications (0); diagnostic imaging (1)|||diagnostic imaging (0)||diagnostic imaging (0)||complications (0)||diagnostic imaging (0)|diagnostic imaging (0)|diagnostic imaging (0)|complications (0)|diagnostic imaging (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-19 | 2016-11-23 | pubmed: 1975-12-1; medline: 1975-12-1 0:1; entrez: 1975-12-1 0:0 | pubmed: 2527 | Cerebrovascular Disorders | ['Cerebrovascular Disorders'] |
2,820 | 1 | Surgical management of severe aortic coarctation and interrupted aortic arch in neonates. | MEDLINE | Manual | NLM | Forty-four infants, 2 to 90 days of age, with severe obstructive lesions of the aortic arch, underwent emergency surgical correction between Jan. 1, 1966, and April 1, 1975. The typical clinical presentation was severe congestive heart failure and acidemia. Resection of an aortic coarctation with end-to-end anastomosis was performed in 31 patients. Eight (26 per cent) died after the operation. Since 1969, the mortality rate has been reduced to 14 per cent (3 of 22 patients) even though the incidence of major associated cardiac lesions has remained essentially constant (56 per cent from 1966 through 1969, 64 per cent from 1970 through March, 1975). This suggests that the higher survival rate has resulted from improved surgical techniques and postoperative care. The mortality rate in the infants operated upon during the second and third months of life was twice as high as that in those operated upon before the age of 1 month. Eight patients with Type A interrupted aortic arch were operated upon and 5 survived. Five patients with Type B aortic arch were operated upon and 3 survived. | The Journal of thoracic and cardiovascular surgery | 0022-5223 | Print | 71 | 1 | Print | 1,976 | Jan | null | 35-48 | N H Fishman (NH); M H Bronstein (MH); W Berman (W); B B Roe (BB); L H Edmunds (LH); S J Robinson (SJ); A M Rudolph (AM) | Journal Article (D016428) | null | Aorta (UI: D001011, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: Yes); Aortic Coarctation (UI: D001017, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); mortality (UI: Q000401, Major: No); surgery (UI: Q000601, Major: Yes); Heart Defects, Congenital (UI: D006330, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); mortality (UI: Q000401, Major: No); surgery (UI: Q000601, Major: Yes); Heart Failure (UI: D006333, Major: No) - Qualifiers: etiology (UI: Q000209, Major: No); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Infant (UI: D007223, Major: No); Infant, Newborn (UI: D007231, Major: No) | Aorta|Aortic Coarctation|Heart Defects, Congenital|Heart Failure|Humans|Hydrogen-Ion Concentration|Infant|Infant, Newborn | abnormalities (1)|complications (0); mortality (0); surgery (1)|complications (0); mortality (0); surgery (1)|etiology (0)|||| | 0|0|0|0|0|0|0|0 | null | 1976-04-15 | 2007-11-15 | pubmed: 1976-1-1; medline: 2001-3-28 10:1; entrez: 1976-1-1 0:0 | pubmed: 2820 | Heart Failure | [] |
2,821 | 1 | Pharmacological analysis of the adrenergic control of the cerebral circulation. | MEDLINE | Manual | NLM | The adrenergic control of the cerebral circulation was subjected to pharmacological analysis. The status of the cerebral circulation was assessed using radioisotope, electromagnetic and resistographic methods. EEG, ECG and arterial pressure were recorded. The acid-base equilibrium and oxygen tension were measured in the arterial blood and cerebrospinal fluid. The experiments showed that the sympathetic innervation plays an important role in controlling cerebral circulation and in the development of cerebrovascular disorders. This was indicated by the constriction of intracranial arteries induced by noradrenaline, stimulation of sympathetic nerves, reflex sympathetic activations and the effect of potassium chloride on the centrol nervous system. The pharmacological study demonstrated that constriction of the intracranial vessels is brought about by an activation of the sympatho-adrenal system which is mediated via alpha-adrenoreceptors of cerebral blood vessels. | Medical biology | 0302-2137 | Print | 53 | 6 | Print | 1,975 | Dec | null | 493-500 | R S Mirzoyan (RS) | Journal Article (D016428) | Phenoxybenzamine (Registry: 0TTZ664R7Z, UI: D010643); Dihydroergotoxine (Registry: 11032-41-0, UI: D004088); Potassium Chloride (Registry: 660YQ98I10, UI: D011189); Propranolol (Registry: 9Y8NXQ24VQ, UI: D011433); Nialamide (Registry: T2Q0RYM725, UI: D009526); Norepinephrine (Registry: X4W3ENH1CV, UI: D009638); Guanethidine (Registry: ZTI6C33Q2Q, UI: D006145) | Acid-Base Equilibrium (UI: D000136, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Animals (UI: D000818, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Cats (UI: D002415, Major: No); Cerebrovascular Circulation (UI: D002560, Major: Yes) - Qualifiers: drug effects (UI: Q000187, Major: No); Cerebrovascular Disorders (UI: D002561, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Dihydroergotoxine (UI: D004088, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Dogs (UI: D004285, Major: No); Electric Stimulation (UI: D004558, Major: No); Guanethidine (UI: D006145, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Nialamide (UI: D009526, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Norepinephrine (UI: D009638, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Partial Pressure (UI: D010313, Major: No); Phenoxybenzamine (UI: D010643, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Potassium Chloride (UI: D011189, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Propranolol (UI: D011433, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Vasomotor System (UI: D014666, Major: Yes) - Qualifiers: drug effects (UI: Q000187, Major: No) | Acid-Base Equilibrium|Animals|Blood Pressure|Cats|Cerebrovascular Circulation|Cerebrovascular Disorders|Dihydroergotoxine|Dogs|Electric Stimulation|Guanethidine|Hydrogen-Ion Concentration|Nialamide|Norepinephrine|Partial Pressure|Phenoxybenzamine|Potassium Chloride|Propranolol|Vasomotor System | drug effects (0)||drug effects (0)||drug effects (0)|physiopathology (0)|pharmacology (0)|||pharmacology (0)||pharmacology (0)|pharmacology (0)||pharmacology (0)|pharmacology (0)|pharmacology (0)|drug effects (0) | 0|0|0|0|1|0|0|0|0|0|0|0|0|0|0|0|0|1 | null | 1976-04-09 | 2013-11-21 | pubmed: 1975-12-1; medline: 1975-12-1 0:1; entrez: 1975-12-1 0:0 | pubmed: 2821 | Cerebrovascular Disorders | ['Cerebrovascular Disorders'] |
2,928 | 1 | Canine cardiac lymph potassium, pH and flow after experimental myocardial infarction. | MEDLINE | Manual | NLM | Canine cardiac lymph was studied after acute experimental myocardial infarction. The lymph potassium concentration remained the same, the lymph potassium content increased, the lymph pH decreased, and the lymph flow increased while the serum potassium and pH remained the same. It is suggested that localized hypoxia may result in cellular changes that release substances, e.g., potassium, to the interstitial space where they mobilize fluid and enhance lymph flow. | Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) | 0037-9727 | Print | 151 | 1 | Print | 1,976 | Jan | null | 146-8 | H N Uhley (HN); S E Leeds (SE); F R Elevitch (FR) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Potassium (Registry: RWP5GA015D, UI: D011188) | Animals (UI: D000818, Major: No); Dogs (UI: D004285, Major: No); Endocardium (UI: D004699, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: Yes); Lymph Nodes (UI: D008198, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); physiology (UI: Q000502, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Potassium (UI: D011188, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); metabolism (UI: Q000378, Major: Yes) | Animals|Dogs|Endocardium|Hydrogen-Ion Concentration|Lymph Nodes|Myocardial Infarction|Potassium | ||||metabolism (1); physiology (0)|metabolism (1)|blood (0); metabolism (1) | 0|0|0|1|0|0|0 | null | 1976-04-09 | 2020-09-30 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 2928; doi: 10.3181/00379727-151-39162 | Myocardial Ischemia | ['Myocardial Infarction'] |
2,973 | 1 | [Prinzmetal angina: clinical aspects and coronarographic findings]. | MEDLINE | Manual | NLM | The clinical course and coronary arteriographic findings in 5 patients with Prinzmetal's variant angina pectoris are reviewed. In 4 patients who had ST-elevations inferiorly, 1 had minimal, 1 only slight, and 1 medium coronary artery disease; 1 had coronary spasm. 1 patient with ST-elevation anteriorly had severe stenosis of the anterior descending coronary artery. All 5 patients had normal left ventriculograms, 3 also had normal left enddiastolic pressure, and 2 slight elevation. Medical treatment was carried out in 2 patients and surgical revascularization in 2. Both treatments were accompanied by marked symptomatic improvement. Spontaneous loss of angina occurred in 1 patient. Prinzmetal's variant angina pectoris may be accompanied by a variety of coronary arteriographic findings and the prognosis appears to be more favorable than previously reported. | Schweizerische medizinische Wochenschrift | 0036-7672 | Print | 106 | 5 | Print | 1,976 | Jan | 31 | 141-6 | I Renggli (I); F Burkart (F) | English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Nitroglycerin (Registry: G59M7S0WS3, UI: D005996) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Adult (UI: D000328, Major: No); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: Yes); drug therapy (UI: Q000188, Major: No); surgery (UI: Q000601, Major: No); Arterial Occlusive Diseases (UI: D001157, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); Coronary Angiography (UI: D017023, Major: Yes); Coronary Artery Bypass (UI: D001026, Major: No); Female (UI: D005260, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Nitroglycerin (UI: D005996, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No) | Adrenergic beta-Antagonists|Adult|Angina Pectoris|Arterial Occlusive Diseases|Coronary Angiography|Coronary Artery Bypass|Female|Humans|Male|Middle Aged|Nitroglycerin | therapeutic use (0)||diagnosis (1); drug therapy (0); surgery (0)|diagnosis (0)|||||||therapeutic use (0) | 0|0|0|0|1|0|0|0|0|0|0 | null | 1976-04-27 | 2013-11-21 | pubmed: 1976-1-31; medline: 1976-1-31 0:1; entrez: 1976-1-31 0:0 | pubmed: 2973 | Myocardial Ischemia | ['Angina Pectoris'] |
3,026 | 1 | [The correlation between activity of enzymes participating in the formation and utilization of acetyl CoA in rabbit heart mitochondria in myocarditis and normal state]. | MEDLINE | Manual | NLM | Activities in rabbit heart mitochondria of acetoacetyl-CoA-thyolase, pyruvate dehydrogenase, acetyl CoA-synthetase, citrate synthase and acetyl carnitine transferase were compared. These enzymes participate in formation and utilization of acetyl-CoA. The acetoacetyl-CoA-thyolase and acetyl CoA-synthetase were shown to possess the more distinct capacity in vitro to form acetyl CoA. The co-enzyme was most efficiently utilized under these experimental conditions by the citrate synthase. The enzymes studied were localized within the mitochondria fraction in both the subfractions of soluble and membrane-bound proteins. In myocarditis a distinct decrease in activities of the acetoacetyl-CoA-thyolase and citrate synthase was observed. | Voprosy meditsinskoi khimii | 0042-8809 | Print | 21 | 6 | Print | null | null | null | 625-9 | E V Sharkova (EV) | English Abstract (D004740); Journal Article (D016428) | Pyruvate Dehydrogenase Complex (Registry: 0, UI: D011768); Acetyl Coenzyme A (Registry: 72-89-9, UI: D000105); Acetyltransferases (Registry: EC 2.3.1.-, UI: D000123); Acetyl-CoA C-Acetyltransferase (Registry: EC 2.3.1.9, UI: D000101); Citrate (si)-Synthase (Registry: EC 2.3.3.1, UI: D002950); Coenzyme A (Registry: SAA04E81UX, UI: D003065) | Acetyl Coenzyme A (UI: D000105, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Acetyl-CoA C-Acetyltransferase (UI: D000101, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Acetyltransferases (UI: D000123, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Animals (UI: D000818, Major: No); Citrate (si)-Synthase (UI: D002950, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Coenzyme A (UI: D003065, Major: No) - Qualifiers: analogs & derivatives (UI: Q000031, Major: Yes); Mitochondria, Muscle (UI: D008931, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Myocarditis (UI: D009205, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Pyruvate Dehydrogenase Complex (UI: D011768, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Rabbits (UI: D011817, Major: No) | Acetyl Coenzyme A|Acetyl-CoA C-Acetyltransferase|Acetyltransferases|Animals|Citrate (si)-Synthase|Coenzyme A|Mitochondria, Muscle|Myocarditis|Myocardium|Pyruvate Dehydrogenase Complex|Rabbits | metabolism (1)|metabolism (0)|metabolism (0)||metabolism (0)|analogs & derivatives (1)|metabolism (1)|metabolism (1)|metabolism (1)|metabolism (0)| | 0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-23 | 2013-11-21 | pubmed: 1975-11-1; medline: 1975-11-1 0:1; entrez: 1975-11-1 0:0 | pubmed: 3026 | Cardiomyopathies | ['Myocarditis'] |
3,073 | 1 | [Findings of subpartal monitoring, status of the newborn infant and evaluation of cardiotocographic findings]. | MEDLINE | Manual | NLM | The parameters of the intrapartal fetal CTG and the actual pH are related to each other and to the Apgar score of the newborn. The interpretation was carried out by means of groups of 300 to 600 cases. The actual fetal pH has the most compact relation to the Apgar score of the newborn (C equals 0,31). But also this contingence is unsatisfactory. At fetal acidosis most of the Apgar scores are pathological, in that manner the pH is the most important test for indication of operative delivery. The rare CTG pattern as dip II and variable decelerations combined with tachycardia of bradycardia, the bradycardia with 80 bpm or less, are likewise indications of urgent delivery. | Zentralblatt fur Gynakologie | 0044-4197 | Print | 98 | 1 | Print | 1,976 | null | null | 3-9 | V Bollmann (V); E P Issel (EP); H Halle (H); D Ballauf (D); C Füssel (C) | English Abstract (D004740); Journal Article (D016428) | null | Acidosis (UI: D000138, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); Apgar Score (UI: D001034, Major: No); Bradycardia (UI: D001919, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); Female (UI: D005260, Major: No); Fetal Blood (UI: D005312, Major: No); Fetal Diseases (UI: D005315, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: Yes); Fetal Heart (UI: D005318, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Heart Rate (UI: D006339, Major: No); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Infant, Newborn (UI: D007231, Major: Yes); Obstetric Labor Complications (UI: D007744, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); Pregnancy (UI: D011247, Major: No); Prenatal Diagnosis (UI: D011296, Major: No); Tachycardia (UI: D013610, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); Uterine Contraction (UI: D014590, Major: No) | Acidosis|Apgar Score|Bradycardia|Female|Fetal Blood|Fetal Diseases|Fetal Heart|Heart Rate|Humans|Hydrogen-Ion Concentration|Infant, Newborn|Obstetric Labor Complications|Pregnancy|Prenatal Diagnosis|Tachycardia|Uterine Contraction | diagnosis (0)||diagnosis (0)|||diagnosis (1)|physiopathology (0)|||||diagnosis (0)|||diagnosis (0)| | 0|0|0|0|0|0|0|0|0|0|1|0|0|0|0|0 | null | 1976-04-27 | 2008-02-11 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 3073 | Arrhythmias, Cardiac | ['Bradycardia', 'Tachycardia'] |
3,096 | 1 | Factors of importance for the degree of ischemic injury in the isolated rat heart. | MEDLINE | Manual | NLM | Isolated working rat hearts were made ischemic by introducing a one-way aortic ball valve. After the ischemic period the hearts were perfused in a retrograde non-working way for 30 min. Flow rates, glycogen, ATP, and creatine-phosphate went down during the time of ischemia, whereas tissue lactate accumulated. For shorter periods of ischemia these values were normalized but after 30 min of ischemia the hearts seemed to be irreversibly damaged. There was a leakage of GOT, GPT, LDH, and CPK from all hearts when ischemic from 5 to 30 min. Different factors that might be of importance for the degree of ischemic injury were tested. The injury tended to be more severe at higher heart rates. Addition of adrenaline 10(-6)M resulted in excessive myocardial damage. A variation of pH from 7.1 to 7.7 did not alter the effects of the ischemic injury. One group of rats were injected with adrenaline for 8 weeks to simulate chronic stress. When hearts from these rats were made ischemic they were more prone to fail compared to controls. The failing hearts, on the other hand, had a lower leakage of enzymes, possibly due to a less severe myocardial damage. A high mechanical performance and a normal noradrenaline content of the hearts are key factors for the development of myocardial infarction, as indicated by this study. | Acta medica Scandinavica. Supplementum | 0365-463X | Print | 587 | null | Print | 1,976 | null | null | 141-9 | A P Waldenstrõm (AP); A C Hjalmarson (AC) | Journal Article (D016428) | Lactates (Registry: 0, UI: D007773); Phosphocreatine (Registry: 020IUV4N33, UI: D010725); Adenosine Triphosphate (Registry: 8L70Q75FXE, UI: D000255); Glycogen (Registry: 9005-79-2, UI: D006003) | Adenosine Triphosphate (UI: D000255, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Animals (UI: D000818, Major: No); Coronary Circulation (UI: D003326, Major: No); Coronary Disease (UI: D003327, Major: Yes) - Qualifiers: metabolism (UI: Q000378, Major: No); physiopathology (UI: Q000503, Major: No); Glycogen (UI: D006003, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Heart Rate (UI: D006339, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Lactates (UI: D007773, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Male (UI: D008297, Major: No); Perfusion (UI: D010477, Major: No); Phosphocreatine (UI: D010725, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Rats (UI: D051381, Major: No) | Adenosine Triphosphate|Animals|Coronary Circulation|Coronary Disease|Glycogen|Heart|Heart Rate|Hydrogen-Ion Concentration|Lactates|Male|Perfusion|Phosphocreatine|Rats | metabolism (0)|||metabolism (0); physiopathology (0)|metabolism (0)|physiopathology (0)|||metabolism (0)|||metabolism (0)| | 0|0|0|1|0|0|0|0|0|0|0|0|0 | null | 1976-04-30 | 2019-09-11 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 3096; doi: 10.1111/j.0954-6820.1976.tb05876.x | Myocardial Ischemia | ['Coronary Disease'] |
3,095 | 1 | Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. | MEDLINE | Manual | NLM | A number of hemodynamic, pharmacologic and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, external counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (elevation of coronary perfusion pressure by alpha-adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (mannitol, hypertonic glucose); presumably by augmenting anaerobic metabolism (glucose-insulin-potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia) or through reduction of collateral flow (hemorrhagic hypotension, minoxidil) or by decreasing substrate availability glycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin, intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, suggesting that the concept of reduction in infarct size following coronary occlusion is applicable clinically. | Acta medica Scandinavica. Supplementum | 0365-463X | Print | 587 | null | Print | 1,976 | null | null | 125-36 | P R Maroko (PR); E Braunwald (E) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Adrenergic alpha-Agonists (Registry: 0, UI: D000316); Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Isoproterenol (Registry: L628TT009W, UI: D007545) | Acute Disease (UI: D000208, Major: No); Adrenergic alpha-Agonists (UI: D000316, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: No); Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: No); Animals (UI: D000818, Major: No); Assisted Circulation (UI: D001243, Major: No); Dogs (UI: D004285, Major: No); Hemodynamics (UI: D006439, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: No); Myocardial Infarction (UI: D009203, Major: Yes) - Qualifiers: drug therapy (UI: Q000188, Major: No); metabolism (UI: Q000378, Major: No); physiopathology (UI: Q000503, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); pathology (UI: Q000473, Major: No); Necrosis (UI: D009336, Major: No); Oxygen Consumption (UI: D010101, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No) | Acute Disease|Adrenergic alpha-Agonists|Adrenergic beta-Antagonists|Animals|Assisted Circulation|Dogs|Hemodynamics|Humans|Isoproterenol|Myocardial Infarction|Myocardium|Necrosis|Oxygen Consumption | |pharmacology (0); therapeutic use (0)|pharmacology (0); therapeutic use (0)||||drug effects (0)||pharmacology (0); therapeutic use (0)|drug therapy (0); metabolism (0); physiopathology (0)|metabolism (1); pathology (0)||drug effects (0) | 0|0|0|0|0|0|0|0|0|1|0|0|0 | null | 1976-04-30 | 2019-09-11 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 3095; doi: 10.1111/j.0954-6820.1976.tb05874.x | Myocardial Ischemia | ['Myocardial Infarction'] |
3,098 | 1 | Double-blind study of the effect of cardioselective beta-blockade on chest pain in acute myocardial infarction. | MEDLINE | Manual | NLM | A double-blind study including three different cardioselective beta-blockers, practolol, H 87/07 and metoprolol, was performed in 54 patients with acute myocardial infarction and chest pain shortly after onset of symptoms. Transmural infarctions were found in 42 patients while 12 patients had nontransmural infarctions. Chest pain and the product of heart rate and systolic blood pressure were significantly reduced in the beta-blocker groups whereas no changes were seen after saline. All patients with nontransmural infarctions and 14 out of 29 with transmural infarctions got pain relief lasting for at least 30 min. None of the patients developed signs of left ventricular backward failure, shock, or bradycardia. A decrease in ST segment elevation was observed in all the transmural infarctions after beta-blockade. No changes in ST segment elevation were found after analgesics when given after saline, but in some cases an increase was seen in this parameter when analgesics were given due to insufficient pain relief after beta-blockers or due to return of chest pain. It is suggested that pain relief by beta-blockers indicates decrease of myocardial ischemia. | Acta medica Scandinavica. Supplementum | 0365-463X | Print | 587 | null | Print | 1,976 | null | null | 201-8 | F Waagstein (F); A C Hjalmarson (AC) | Clinical Trial (D016430); Journal Article (D016428); Randomized Controlled Trial (D016449) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Propanolamines (Registry: 0, UI: D011412); Practolol (Registry: SUG9176GRW, UI: D011217) | Acute Disease (UI: D000208, Major: No); Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Clinical Trials as Topic (UI: D002986, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Middle Aged (UI: D008875, Major: No); Myocardial Contraction (UI: D009200, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); Pain (UI: D010146, Major: No); Practolol (UI: D011217, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes) | Acute Disease|Adrenergic beta-Antagonists|Blood Pressure|Clinical Trials as Topic|Heart Rate|Humans|Middle Aged|Myocardial Contraction|Myocardial Infarction|Pain|Practolol|Propanolamines | |pharmacology (0); therapeutic use (1)|drug effects (0)||drug effects (0)|||drug effects (0)|drug therapy (1)||pharmacology (0); therapeutic use (0)|pharmacology (0); therapeutic use (1) | 0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-30 | 2019-09-11 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 3098; doi: 10.1111/j.0954-6820.1976.tb05882.x | Myocardial Ischemia | ['Myocardial Infarction'] |
3,150 | 1 | Kawasaki disease. Relationship with infantile periarteritis nodosa. | MEDLINE | Manual | NLM | Until 1972, Kawasaki disease, or acute febrile infantile mucocutaneous lymph node syndrome (MCLS), was considered in Japan to be a nonfatal disease with a favorable prognosis. Based on the findings from two autopsy cases of MCLS, we believe that sudden and unexpected death during convalescence may be due to arterial lesions, especially those involving the coronary artery, that resemble those of periarteritis nodosa. Of 29 autopsy cases of MCLS, gathered from all over Japan, all exhibited arteritis lesions (eg, aneurysm due to coronary arteritis). Such vascular pathological findings may in fact represent the same entity as infantile periarteritis nodosa. Whether infantile periarteritis nodosa can be identified with the adult type is still debatable. The particular manifestations of infantile periarteritis nodosa might be related to severe vasculitis. Autopsy cases of infantile periarteritis nodosa without MCLS manifestations are being collected and studied. | Archives of pathology & laboratory medicine | 0003-9985 | Print | 100 | 2 | Print | 1,976 | Feb | null | 81-6 | N Tanaka (N); K Sekimoto (K); S Naoe (S) | Journal Article (D016428) | null | Age Factors (UI: D000367, Major: No); Child (UI: D002648, Major: No); Child, Preschool (UI: D002675, Major: No); Coronary Vessels (UI: D003331, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No); Edema, Cardiac (UI: D004489, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No); Erythema (UI: D004890, Major: No) - Qualifiers: mortality (UI: Q000401, Major: No); pathology (UI: Q000473, Major: No); Female (UI: D005260, Major: No); Heart Aneurysm (UI: D006322, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No); Humans (UI: D006801, Major: No); Infant (UI: D007223, Major: No); Japan (UI: D007564, Major: No); Lymphatic Diseases (UI: D008206, Major: No) - Qualifiers: mortality (UI: Q000401, Major: No); pathology (UI: Q000473, Major: Yes); Male (UI: D008297, Major: No); Polyarteritis Nodosa (UI: D010488, Major: No) - Qualifiers: mortality (UI: Q000401, Major: No); pathology (UI: Q000473, Major: Yes); Renal Artery (UI: D012077, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No); Syndrome (UI: D013577, Major: No); Thymus Gland (UI: D013950, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No) | Age Factors|Child|Child, Preschool|Coronary Vessels|Edema, Cardiac|Erythema|Female|Heart Aneurysm|Humans|Infant|Japan|Lymphatic Diseases|Male|Polyarteritis Nodosa|Renal Artery|Syndrome|Thymus Gland | |||pathology (0)|pathology (0)|mortality (0); pathology (0)||pathology (0)||||mortality (0); pathology (1)||mortality (0); pathology (1)|pathology (0)||pathology (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-04-30 | 2004-11-17 | pubmed: 1976-2-1; medline: 1976-2-1 0:1; entrez: 1976-2-1 0:0 | pubmed: 3150 | Cardiomyopathies | ['Edema, Cardiac'] |
3,241 | 1 | [Role of P50 in resuscitation (author's transl)]. | MEDLINE | Manual | NLM | The amount of oxygen made available to the tissues of the body depends essentially upon pulmonary gas exchanges, cardiac output and its regional distribution, haemoglobin concentration and also upon the oxygen affinity of the haemoglobin molecule. That a standard oxyhaemoglobin dissociation curve faithfully describes oxygen loading and unloading both in healthy subjects and in those suffering from pathological process has come under attack. Beside the effect of pH, PCO2 and temperature, the oxyhaemoglobin dissociation curve can be modified by alterations of other factors (concentration of 2,3-diphosphoglycerate, hormones, drugs). Although the shifts of the oxyhaemoglobin dissociation curve, expressed by variations of P50 may seem minute, the effect of these shifts, expressed in terms of the ""functional value of haemoglobin"" are very large. Assessment of the intensive care patient must take into account the effect of alterations of the oxyhaemoglobin dissociation curve which can either increase or diminish tissue oxygenation. | Bulletin de physio-pathologie respiratoire | 0007-439X | Print | 11 | 5 | Print | null | null | null | 637-58 | P Foëx (P) | Journal Article (D016428); Review (D016454) | Carbon Dioxide (Registry: 142M471B3J, UI: D002245) | Blood (UI: D001769, Major: No); Carbon Dioxide (UI: D002245, Major: No) - Qualifiers: physiology (UI: Q000502, Major: No); Cardiac Output (UI: D002302, Major: No); Cardiovascular Diseases (UI: D002318, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Diabetes Mellitus (UI: D003920, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Extracorporeal Circulation (UI: D005112, Major: No); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Hypoxia (UI: D000860, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Kidney Failure, Chronic (UI: D007676, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Respiratory Tract Diseases (UI: D012140, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Resuscitation (UI: D012151, Major: Yes); Shock (UI: D012769, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No) | Blood|Carbon Dioxide|Cardiac Output|Cardiovascular Diseases|Coronary Disease|Diabetes Mellitus|Extracorporeal Circulation|Humans|Hydrogen-Ion Concentration|Hypoxia|Kidney Failure, Chronic|Respiratory Tract Diseases|Resuscitation|Shock | |physiology (0)||physiopathology (0)|physiopathology (0)|physiopathology (0)||||physiopathology (0)|physiopathology (0)|physiopathology (0)||physiopathology (0) | 0|0|0|0|0|0|0|0|0|0|0|0|1|0 | null | 1976-05-18 | 2016-11-23 | pubmed: 1975-9-1; medline: 1975-9-1 0:1; entrez: 1975-9-1 0:0 | pubmed: 3241 | Myocardial Ischemia | ['Coronary Disease'] |
3,242 | 1 | [Isotopic study of fluid and electrolyte disturbances in decompensated chronic respiratory insufficiency (author's transl)]. | MEDLINE | Manual | NLM | The study of fluid and electrolyte disturbances by isotope radiodilution method is carried out in 22 patients with chronic respiratory insufficiency and cardiac failure. The simultaneous measurements of hydro-ionic compartments have been carried out with tritiated water (HTO), labelled sodium (22Na), labelled potassium (42K) and labelled bromine (82Br). From these measurements, the various water spaces are calculated: total water (ET) and extracellular fluids (LEC), also exchangeable electrolytes: sodium (NaE), potassium (KE), chlorine (ClE) and derived values. Results are compared to corresponding values in controls with the same obesity index. Patients with respiratory insufficiency show a fluid and sodium rise, similar to that found in cardiac failure and denutrition. The (NaE + KE)/ET ratio is not significantly decreased and the natremia is only slightly lower. There is no real potassium depletion in most patients. | Bulletin de physio-pathologie respiratoire | 0007-439X | Print | 11 | 5 | Print | null | null | null | 683-707 | F Wattel (F); J Lefèvre (J); C Chopin (C); D Lottin (D); B Raviart (B) | English Abstract (D004740); Journal Article (D016428) | Carbon Dioxide (Registry: 142M471B3J, UI: D002245); Chlorine (Registry: 4R7X1O2820, UI: D002713); Sodium (Registry: 9NEZ333N27, UI: D012964); Potassium (Registry: RWP5GA015D, UI: D011188); Oxygen (Registry: S88TT14065, UI: D010100) | Aged (UI: D000368, Major: No); Blood (UI: D001769, Major: No); Body Water (UI: D001834, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Carbon Dioxide (UI: D002245, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Chlorine (UI: D002713, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Extracellular Space (UI: D005110, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Middle Aged (UI: D008875, Major: No); Obesity (UI: D009765, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Oxygen (UI: D010100, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Potassium (UI: D011188, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Respiratory Insufficiency (UI: D012131, Major: No) - Qualifiers: complications (UI: Q000150, Major: Yes); Sodium (UI: D012964, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Water-Electrolyte Imbalance (UI: D014883, Major: No) - Qualifiers: etiology (UI: Q000209, Major: Yes) | Aged|Blood|Body Water|Carbon Dioxide|Chlorine|Coronary Disease|Extracellular Space|Humans|Hydrogen-Ion Concentration|Middle Aged|Obesity|Oxygen|Potassium|Respiratory Insufficiency|Sodium|Water-Electrolyte Imbalance | ||metabolism (0)|blood (0)|metabolism (0)|metabolism (0)|metabolism (0)||||complications (0)|blood (0)|metabolism (0)|complications (1)|metabolism (0)|etiology (1) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-05-18 | 2013-11-21 | pubmed: 1975-9-1; medline: 1975-9-1 0:1; entrez: 1975-9-1 0:0 | pubmed: 3242 | Myocardial Ischemia | ['Coronary Disease'] |
3,293 | 1 | Contribution of tissue acidosis to ischemic injury in the perfused rat heart. | MEDLINE | Manual | NLM | The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed. | Circulation | 0009-7322 | Print | 53 | 3 Suppl | Print | 1,976 | Mar | null | I3-14 | J R Williamson (JR); S W Schaffer (SW); C Ford (C); B Safer (B) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Adenine Nucleotides (Registry: 0, UI: D000227); Fatty Acids (Registry: 0, UI: D005227); Fructosephosphates (Registry: 0, UI: D005636); Glucosephosphates (Registry: 0, UI: D005958); Lactates (Registry: 0, UI: D007773); Pyruvates (Registry: 0, UI: D011773); Phosphocreatine (Registry: 020IUV4N33, UI: D010725); NAD (Registry: 0U46U6E8UK, UI: D009243); Adenosine Monophosphate (Registry: 415SHH325A, UI: D000249); NADP (Registry: 53-59-8, UI: D009249); Glucose (Registry: IY9XDZ35W2, UI: D005947) | Acidosis, Respiratory (UI: D000142, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); physiopathology (UI: Q000503, Major: No); Adenine Nucleotides (UI: D000227, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Adenosine Monophosphate (UI: D000249, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Animals (UI: D000818, Major: No); Coronary Circulation (UI: D003326, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); physiopathology (UI: Q000503, Major: No); Cytosol (UI: D003600, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Fatty Acids (UI: D005227, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Fructosephosphates (UI: D005636, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Glucose (UI: D005947, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Glucosephosphates (UI: D005958, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Heart Ventricles (UI: D006352, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); In Vitro Techniques (UI: D066298, Major: No); Lactates (UI: D007773, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Male (UI: D008297, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); NAD (UI: D009243, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); NADP (UI: D009249, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Oxygen Consumption (UI: D010101, Major: No); Phosphocreatine (UI: D010725, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Pressure (UI: D011312, Major: No); Pyruvates (UI: D011773, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Rats (UI: D051381, Major: No) | Acidosis, Respiratory|Adenine Nucleotides|Adenosine Monophosphate|Animals|Coronary Circulation|Coronary Disease|Cytosol|Fatty Acids|Fructosephosphates|Glucose|Glucosephosphates|Heart Ventricles|Hydrogen-Ion Concentration|In Vitro Techniques|Lactates|Male|Myocardium|NAD|NADP|Oxygen Consumption|Phosphocreatine|Pressure|Pyruvates|Rats | metabolism (1); physiopathology (0)|metabolism (0)|metabolism (0)|||metabolism (1); physiopathology (0)|metabolism (0)|metabolism (0)|metabolism (0)|metabolism (0)|metabolism (0)|physiopathology (0)|||metabolism (0)||metabolism (1)|metabolism (0)|metabolism (0)||metabolism (0)||metabolism (0)| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-05-25 | 2014-11-20 | pubmed: 1976-3-1; medline: 1976-3-1 0:1; entrez: 1976-3-1 0:0 | pubmed: 3293 | Myocardial Ischemia | ['Coronary Disease'] |
3,420 | 1 | Anti-arrhythmic action of nadolol, a beta-adrenergic receptor blocking agent. | MEDLINE | Manual | NLM | The anti-arrhythmic action of 2,3-cis-1,2,3,4-tetrahydro-5-[(2-hydroxy-3-tert-butylamino)propoxy]2,3-naphthalenediol (nadolol) was evaluated and compared with that of propranolol in several experimental models of cardiac arrhythmias. Both nadolol and propranolol antagonized isoproterenol-induced tachycardia and ouabain-induced arrhythmias in cats, antagonized coronary artery ligation-induced ventricular fibrillation and suppressed ventricular ectopic activity during vagal stimulation in dogs. In contrast to propranolol, nadolol was considerably weaker in suppressing existing digoxin-induced arrhythmias, lacked local anesthetic activity and did not depress the heart in dogs. Because of these findings, it is concluded that the anti-arrhythmic activity of nadolol is apparently related to blockade of beta-adrenergic receptors. | European journal of pharmacology | 0014-2999 | Print | 35 | 1 | Print | 1,976 | Jan | null | 17-27 | D B Evans (DB); M T Peschka (MT); R J Lee (RJ); R J Laffan (RJ) | Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Anti-Arrhythmia Agents (Registry: 0, UI: D000889); Naphthols (Registry: 0, UI: D009284); Propanolamines (Registry: 0, UI: D011412); Ouabain (Registry: 5ACL011P69, UI: D010042); Isoproterenol (Registry: L628TT009W, UI: D007545) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Animals (UI: D000818, Major: No); Anti-Arrhythmia Agents (UI: D000889, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Arrhythmias, Cardiac (UI: D001145, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); Dogs (UI: D004285, Major: No); Electric Stimulation (UI: D004558, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Heart Conduction System (UI: D006329, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); Male (UI: D008297, Major: No); Naphthols (UI: D009284, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Neural Conduction (UI: D009431, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Ouabain (UI: D010042, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Vagus Nerve (UI: D014630, Major: No) - Qualifiers: physiology (UI: Q000502, Major: No); Ventricular Fibrillation (UI: D014693, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No) | Adrenergic beta-Antagonists|Animals|Anti-Arrhythmia Agents|Arrhythmias, Cardiac|Dogs|Electric Stimulation|Heart|Heart Conduction System|Isoproterenol|Male|Naphthols|Neural Conduction|Ouabain|Propanolamines|Vagus Nerve|Ventricular Fibrillation | pharmacology (1)||pharmacology (1)|chemically induced (0)|||physiopathology (0)|drug effects (0)|antagonists & inhibitors (0)||pharmacology (0)|drug effects (0)|antagonists & inhibitors (0)|pharmacology (1)|physiology (0)|physiopathology (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-06-02 | 2019-06-23 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 3420; pii: 0014-2999(76)90296-X; doi: 10.1016/0014-2999(76)90296-x | Arrhythmias, Cardiac | ['Ventricular Fibrillation'] |
3,643 | 1 | The antiarrhythmic and cardiovascular properties of 1-dimethyl isopropylamino-3-(2-phenylphenoxy)-propan-2-ol chloride, UM-424. | MEDLINE | Manual | NLM | The quarternary ammonium compound, UM-424 [1-dimethyl isopropylamino-3-(2-phenylphenoxy)-propan-2-ol chloride], was evaluated for its antiarrhythmic and hemodynamic effects. UM-424 converted ouabain-induced ventricular tachycardia in the anesthetized dog when administered in an average dose of 4.6 mg/kg i.v. Pretreatment of anesthetized dogs with UM-424, 10 mg/kg, provided complete protection against the development of premature beats and ventricular fibrillation when the left anterior descending coronary artery was occluded for 20 minutes and then released. UM-424 was effective in reversing ventricular arrhythmias in conscious animals which had been subjected to a two-stage ligation of the anterior descending coronary artery. The mean ectopic rate in a group of five dogs was 143 +/- 4.0 (S.E.M.) beats/min 24 hours after coronary ligation. Normal sinus rhythm was restored with a mean dose of 9.5 mg/kg of UM-424 and was maintained for a period in excess of 60 minutes. The ventricular fibrillation threshold was increased from a control value of 4.0 +/- 0.4 to 26.2 +/- 8.6 mA (P less than .05) 30 minutes after pretreatment with UM-424, 10 mg/kg. Inotropic and chronotropic dose-response studies to isoproterenol in the anesthetized dog demonstrated that the quarternary compound lacked beta adrenergic receptor blocking properties. UM-424, 10 mg/kg, did not produce any persistent changes in spontaneous heart rate, cardiac contractile force, left ventricular dP/ct, mean arterial blood pressure, cardiac output and mean pulmonary arterial pressure. | The Journal of pharmacology and experimental therapeutics | 0022-3565 | Print | 196 | 2 | Print | 1,976 | Feb | null | 420-32 | F J Kniffen (FJ); S Winokur (S); R E Counsell (RE); B R Lucchesi (BR) | Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Anti-Arrhythmia Agents (Registry: 0, UI: D000889); Propanolamines (Registry: 0, UI: D011412); Quaternary Ammonium Compounds (Registry: 0, UI: D000644); UM-424 (Registry: 58520-98-2, UI: C011588); Ouabain (Registry: 5ACL011P69, UI: D010042); Isoproterenol (Registry: L628TT009W, UI: D007545) | Adrenergic beta-Antagonists (UI: D000319, Major: No); Animals (UI: D000818, Major: No); Anti-Arrhythmia Agents (UI: D000889, Major: Yes); Arrhythmias, Cardiac (UI: D001145, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); physiopathology (UI: Q000503, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Cardiac Output (UI: D002302, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Cats (UI: D002415, Major: No); Coronary Vessels (UI: D003331, Major: No) - Qualifiers: physiology (UI: Q000502, Major: No); Dogs (UI: D004285, Major: No); Drug Interactions (UI: D004347, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Hemodynamics (UI: D006439, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: Yes); Isoproterenol (UI: D007545, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Ligation (UI: D008026, Major: No); Male (UI: D008297, Major: No); Myocardial Contraction (UI: D009200, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Ouabain (UI: D010042, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Papillary Muscles (UI: D010210, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Quaternary Ammonium Compounds (UI: D000644, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Ventricular Fibrillation (UI: D014693, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No) | Adrenergic beta-Antagonists|Animals|Anti-Arrhythmia Agents|Arrhythmias, Cardiac|Blood Pressure|Cardiac Output|Cats|Coronary Vessels|Dogs|Drug Interactions|Heart Rate|Hemodynamics|Isoproterenol|Ligation|Male|Myocardial Contraction|Ouabain|Papillary Muscles|Propanolamines|Quaternary Ammonium Compounds|Ventricular Fibrillation | |||chemically induced (0); physiopathology (0)|drug effects (0)|drug effects (0)||physiology (0)|||drug effects (0)|drug effects (1)|pharmacology (0)|||drug effects (0)|pharmacology (0)|drug effects (0)|pharmacology (1)|pharmacology (1)|physiopathology (0) | 0|0|1|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-05-10 | 2019-12-10 | pubmed: 1976-2-1; medline: 1976-2-1 0:1; entrez: 1976-2-1 0:0 | pubmed: 3643 | Arrhythmias, Cardiac | ['Ventricular Fibrillation'] |
3,647 | 1 | A new series of cardioselective adrenergic beta-receptor blocking compounds. 1-(2-Acyl-4-acylaminophenoxy)-3-isopropylaminopropan-2-ols. | MEDLINE | Manual | NLM | A series of 1-(2-acyl-4-acylaminophenoxy)-3-isopropylaminopropan-2-ols has been synthesized and examined for beta-receptor blocking and antiarrhythmic activity. Several of these compounds are more than 20 times as active in blocking cardiac beta-receptors than vascular beta-receptors when given intravenously to anesthetized cats. The activities have been correlated quantitatively with partition and steric substitution constants. The observed relationships are consistent with a tentative proposal that the vascular receptor is situated in a more lipophilic environment than the cardiac receptor so that there is a differential transport effect between the two types of receptor. | Journal of medicinal chemistry | 0022-2623 | Print | 19 | 3 | Print | 1,976 | Mar | null | 399-402 | B Basil (B); J R Clark (JR); E C Coffee (EC); R Jordon (R); A H Loveless (AH); D L Pain (DL); K R Wooldridge (KR) | Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Anilides (Registry: 0, UI: D000813); Propanolamines (Registry: 0, UI: D011412); Receptors, Adrenergic (Registry: 0, UI: D011941); Ouabain (Registry: 5ACL011P69, UI: D010042); Isoproterenol (Registry: L628TT009W, UI: D007545) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: chemical synthesis (UI: Q000138, Major: Yes); pharmacology (UI: Q000494, Major: No); Anilides (UI: D000813, Major: No) - Qualifiers: chemical synthesis (UI: Q000138, Major: No); pharmacology (UI: Q000494, Major: No); Animals (UI: D000818, Major: No); Arrhythmias, Cardiac (UI: D001145, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); Cats (UI: D002415, Major: No); Dogs (UI: D004285, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Isoproterenol (UI: D007545, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); Molecular Conformation (UI: D008968, Major: No); Organ Specificity (UI: D009928, Major: No); Ouabain (UI: D010042, Major: No) - Qualifiers: antagonists & inhibitors (UI: Q000037, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: chemical synthesis (UI: Q000138, Major: Yes); pharmacology (UI: Q000494, Major: No); Receptors, Adrenergic (UI: D011941, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Structure-Activity Relationship (UI: D013329, Major: No) | Adrenergic beta-Antagonists|Anilides|Animals|Arrhythmias, Cardiac|Cats|Dogs|Heart Rate|Isoproterenol|Molecular Conformation|Organ Specificity|Ouabain|Propanolamines|Receptors, Adrenergic|Structure-Activity Relationship | chemical synthesis (1); pharmacology (0)|chemical synthesis (0); pharmacology (0)||chemically induced (0)|||drug effects (0)|antagonists & inhibitors (0)|||antagonists & inhibitors (0)|chemical synthesis (1); pharmacology (0)|drug effects (0)| | 0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-05-25 | 2019-07-09 | pubmed: 1976-3-1; medline: 1976-3-1 0:1; entrez: 1976-3-1 0:0 | pubmed: 3647; doi: 10.1021/jm00225a012 | Arrhythmias, Cardiac | [] |
3,889 | 1 | [Extracardiac factors in the development of arrhythmias (author's transl)]. | MEDLINE | Manual | NLM | A brief survey is given of some of the most frequent extracardiac causes which may provoke disturbances of rhythm. The importance of psychogenic and metabolic factors is emphasized. Additional organic lesions cannot be excluded in every case. | Wiener klinische Wochenschrift | 0043-5325 | Print | 87 | 22 | Print | null | null | null | 737-40 | H Mösslacher (H); J Slany (J) | English Abstract (D004740); Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Hypnotics and Sedatives (Registry: 0, UI: D006993); Sympathomimetics (Registry: 0, UI: D013566); Atropine (Registry: 7C0697DR9I, UI: D001285) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Arrhythmias, Cardiac (UI: D001145, Major: No) - Qualifiers: chemically induced (UI: Q000139, Major: No); drug therapy (UI: Q000188, Major: No); etiology (UI: Q000209, Major: Yes); Atropine (UI: D001285, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Central Nervous System Diseases (UI: D002493, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Humans (UI: D006801, Major: No); Hyperthyroidism (UI: D006980, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Hypnotics and Sedatives (UI: D006993, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Neurotic Disorders (UI: D009497, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Psychotherapy (UI: D011613, Major: No); Reflex (UI: D012018, Major: No); Sympathomimetics (UI: D013566, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Water-Electrolyte Imbalance (UI: D014883, Major: No) - Qualifiers: complications (UI: Q000150, Major: No) | Adrenergic beta-Antagonists|Arrhythmias, Cardiac|Atropine|Central Nervous System Diseases|Humans|Hyperthyroidism|Hypnotics and Sedatives|Neurotic Disorders|Psychotherapy|Reflex|Sympathomimetics|Water-Electrolyte Imbalance | therapeutic use (0)|chemically induced (0); drug therapy (0); etiology (1)|therapeutic use (0)|complications (0)||complications (0)|therapeutic use (0)|complications (0)|||therapeutic use (0)|complications (0) | 0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-06-02 | 2013-11-21 | pubmed: 1975-11-1; medline: 1975-11-1 0:1; entrez: 1975-11-1 0:0 | pubmed: 3889 | Arrhythmias, Cardiac | [] |
3,949 | 1 | Pattern of enzyme activity following acute myocardial infarction with special reference to gamma-glutamyl transpeptidase. | MEDLINE | Manual | NLM | The present study on 55 consecutive patients with acute myocardial infarction (AMI) draws attention to the relationship between different enzyme maxima in AMI, with special reference to serum gamma-glutamyl transpeptidase (S-GT). In more than 60% of the patients the S-GT was increased during the hospital stay. The S-GT rise nearly always began during the first days, reached a maximum within 5--8 days and normalized with 2--3 weeks. We failed to find the late increase in S-GT reported by others. The rise of S-GT is particularly common in patients with inferior infarction, with or without right ventricular involvement. We conclude that S-GT activity is not a useful early or late indicator of AMI but a very sensitive test for hepatic dysfunction in patients with AMI. | Acta medica Scandinavica | 0001-6101 | Print | 199 | 3 | Print | 1,976 | null | null | 217-21 | U Säwe (U); L R Erhardt (LR); A Sjögren (A) | Journal Article (D016428) | L-Lactate Dehydrogenase (Registry: EC 1.1.1.27, UI: D007770); gamma-Glutamyltransferase (Registry: EC 2.3.2.2, UI: D005723); Alanine Transaminase (Registry: EC 2.6.1.2, UI: D000410); Creatine Kinase (Registry: EC 2.7.3.2, UI: D003402); Alkaline Phosphatase (Registry: EC 3.1.3.1, UI: D000469) | Acute Disease (UI: D000208, Major: No); Alanine Transaminase (UI: D000410, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Alkaline Phosphatase (UI: D000469, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Creatine Kinase (UI: D003402, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Female (UI: D005260, Major: No); Humans (UI: D006801, Major: No); L-Lactate Dehydrogenase (UI: D007770, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Liver (UI: D008099, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Male (UI: D008297, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: enzymology (UI: Q000201, Major: Yes); physiopathology (UI: Q000503, Major: No); Time Factors (UI: D013997, Major: No); gamma-Glutamyltransferase (UI: D005723, Major: No) - Qualifiers: blood (UI: Q000097, Major: Yes) | Acute Disease|Alanine Transaminase|Alkaline Phosphatase|Creatine Kinase|Female|Humans|L-Lactate Dehydrogenase|Liver|Male|Myocardial Infarction|Time Factors|gamma-Glutamyltransferase | |blood (0)|blood (0)|blood (0)|||blood (0)|physiopathology (0)||enzymology (1); physiopathology (0)||blood (1) | 0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-05-25 | 2019-08-12 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 3949; doi: 10.1111/j.0954-6820.1976.tb06719.x | Myocardial Ischemia | ['Myocardial Infarction'] |
3,959 | 1 | Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. | MEDLINE | Manual | NLM | Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein. | The American journal of cardiology | 0002-9149 | Print | 37 | 4 | Print | 1,976 | Mar | 31 | 501-7 | T J Regan (TJ); R M Effros (RM); B Haider (B); H A Oldewurtel (HA); P O Ettinger (PO); S S Ahmed (SS) | Journal Article (D016428); Research Support, U.S. Gov't, P.H.S. (D013487) | Alkalies (Registry: 0, UI: D000468); Carbonates (Registry: 0, UI: D002254); Cations, Monovalent (Registry: 0, UI: D002414); Edetic Acid (Registry: 9G34HU7RV0, UI: D004492); Dimethadione (Registry: ALU9NPM703, UI: D004114) | Acidosis (UI: D000138, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Alkalies (UI: D000468, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); therapeutic use (UI: Q000627, Major: No); Animals (UI: D000818, Major: No); Body Water (UI: D001834, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Carbonates (UI: D002254, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Cations, Monovalent (UI: D002414, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); metabolism (UI: Q000378, Major: No); physiopathology (UI: Q000503, Major: No); Coronary Vessels (UI: D003331, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Dimethadione (UI: D004114, Major: No); Dogs (UI: D004285, Major: No); Edetic Acid (UI: D004492, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Extracellular Space (UI: D005110, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: Yes); Hydrogen-Ion Concentration (UI: D006863, Major: No); Indicator Dilution Techniques (UI: D007201, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); pathology (UI: Q000473, Major: No) | Acidosis|Alkalies|Animals|Body Water|Carbonates|Cations, Monovalent|Coronary Disease|Coronary Vessels|Dimethadione|Dogs|Edetic Acid|Extracellular Space|Heart|Hydrogen-Ion Concentration|Indicator Dilution Techniques|Myocardium | metabolism (1)|pharmacology (1); therapeutic use (0)||metabolism (0)|pharmacology (0)||drug therapy (0); metabolism (0); physiopathology (0)|drug effects (0)|||pharmacology (0)|metabolism (0)|physiopathology (1)|||metabolism (0); pathology (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-06-02 | 2019-06-22 | pubmed: 1976-3-31; medline: 1976-3-31 0:1; entrez: 1976-3-31 0:0 | pubmed: 3959; pii: 0002-9149(76)90388-X; doi: 10.1016/0002-9149(76)90388-x | Myocardial Ischemia | ['Coronary Disease'] |
3,960 | 1 | Effects of allopurinol, propranolol and methylprednisolone on infarct size in experimental myocardial infarction. | MEDLINE | Manual | NLM | With use of a canine model of occlusion of the left anterior descending coronary artery and an intracellular lactic dehydrogenase stain to measure infarct size directly, the effects of allopurinol, methylprednisolone sodium succinate and propranolol were studied. Allopurinol did not influence the extent of myocardial necrosis, whereas both methylprednisolone and propranolol significantly reduced myocardial infarct size. Possible mechanisms of action and clinical applicability of these agents are discussed. | The American journal of cardiology | 0002-9149 | Print | 37 | 4 | Print | 1,976 | Mar | 31 | 572-80 | C H Shatney (CH); D J MacCarter (DJ); R C Lillehei (RC) | Journal Article (D016428) | Allopurinol (Registry: 63CZ7GJN5I, UI: D000493); Propranolol (Registry: 9Y8NXQ24VQ, UI: D011433); Oxygen (Registry: S88TT14065, UI: D010100); Methylprednisolone (Registry: X4W7ZR7023, UI: D008775) | Allopurinol (UI: D000493, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); therapeutic use (UI: Q000627, Major: No); Animals (UI: D000818, Major: No); Blood (UI: D001769, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Disease Models, Animal (UI: D004195, Major: Yes); Dogs (UI: D004285, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Hemodynamics (UI: D006439, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Methylprednisolone (UI: D008775, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); therapeutic use (UI: Q000627, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: pathology (UI: Q000473, Major: Yes); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Oxygen (UI: D010100, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Propranolol (UI: D011433, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); therapeutic use (UI: Q000627, Major: No) | Allopurinol|Animals|Blood|Coronary Disease|Disease Models, Animal|Dogs|Heart|Hemodynamics|Hydrogen-Ion Concentration|Methylprednisolone|Myocardial Infarction|Myocardium|Oxygen|Propranolol | pharmacology (1); therapeutic use (0)|||drug therapy (0)|||drug effects (0)|drug effects (0)||pharmacology (1); therapeutic use (0)|pathology (1)|metabolism (0)|blood (0)|pharmacology (1); therapeutic use (0) | 0|0|0|0|1|0|0|0|0|0|0|0|0|0 | null | 1976-06-02 | 2019-06-22 | pubmed: 1976-3-31; medline: 1976-3-31 0:1; entrez: 1976-3-31 0:0 | pubmed: 3960; pii: 0002-9149(76)90398-2; doi: 10.1016/0002-9149(76)90398-2 | Myocardial Ischemia | ['Coronary Disease', 'Myocardial Infarction'] |
4,080 | 1 | Effects of the cardioselective beta-adrenergic receptor blocking agent metoprolol in angina pectoris. Subacute study with exercise tests. | MEDLINE | Manual | NLM | The effect of a cardioselective beta-adrenergic blocking agent, metoprolol, on symptoms and exercise tolerance was studied in 16 patients with angina pectoris. Metroprolol was compared with placebo at two dose levels (20 mg t.d.s. and 50 mg t.d.s.) in a double-blind trial in 14 patients. Compared with placebo, metroprolol caused a significant reduction of heart rate and systolic blood pressure during exercise, and consequently a reduction of the rate-pressure product. The reduction was greater with 50 mg t.d.s. than with 20 mg t.d.s. The exercise tolerance measured as total work increased significantly by 21 per cent during treatment with metroprolol 20 mg t.d.s., and by 17 per cent during treatment with 50 mg t.d.s. There was a reduction in the number of anginal attacks and in nitroglycerin consumption, and subjective improvement of angina pectoris at both dose levels of metroprolol. No signs of cardiac failure appeared during any of the four treatment periods. Heart volume showed no significant change. Unwanted effects were of the same frequency and severity during treatment with metroprolol at both dose levels as with placebo. | British heart journal | 0007-0769 | Print | 38 | 2 | Print | 1,976 | Feb | null | 155-61 | L G Ekelund (LG); A G Olsson (AG); L Orö (L); S Rössner (S) | Clinical Trial (D016430); Comparative Study (D003160); Controlled Clinical Trial (D018848); Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Propanolamines (Registry: 0, UI: D011412); Nitroglycerin (Registry: G59M7S0WS3, UI: D005996) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); therapeutic use (UI: Q000627, Major: Yes); Aged (UI: D000368, Major: No); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: Yes); physiopathology (UI: Q000503, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Clinical Trials as Topic (UI: D002986, Major: No); Drug Administration Schedule (UI: D004334, Major: No); Exercise Test (UI: D005080, Major: No); Female (UI: D005260, Major: No); Heart (UI: D006321, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Nitroglycerin (UI: D005996, Major: No) - Qualifiers: administration & dosage (UI: Q000008, Major: No); Propanolamines (UI: D011412, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: Yes) | Adrenergic beta-Antagonists|Aged|Angina Pectoris|Blood Pressure|Clinical Trials as Topic|Drug Administration Schedule|Exercise Test|Female|Heart|Heart Rate|Humans|Male|Middle Aged|Nitroglycerin|Propanolamines | pharmacology (0); therapeutic use (1)||drug therapy (1); physiopathology (0)|drug effects (0)|||||physiopathology (0)|drug effects (0)||||administration & dosage (0)|therapeutic use (1) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2019-05-03 | pubmed: 1976-2-1; medline: 1976-2-1 0:1; entrez: 1976-2-1 0:0 | pubmed: 4080; pmc: PMC482986; doi: 10.1136/hrt.38.2.155 | Myocardial Ischemia | ['Angina Pectoris'] |
4,084 | 1 | The use of a single venous blood sample to assess oxygen binding in haemoglobin. | MEDLINE | Manual | NLM | The measurement of pH, PO2, PCO2 and SO2 in a single venous blood sample can be used to determine the P50 at standard or at in vivo conditions. This technique makes it feasible for a physician, firstly, to make an assessment of the net adaptation of the red cell to reductions in blood oxygen content or flow and, secondly, to make an initial assessment of whether a haemoglobin with altered affinity for oxygen is present in subjects with polycythaemia or anaemia. | British journal of haematology | 0007-1048 | Print | 32 | 1 | Print | 1,976 | Jan | null | 89-98 | M A Lichtman (MA); M Murphy (M); M Pogal (M) | Journal Article (D016428); Research Support, U.S. Gov't, Non-P.H.S. (D013486); Research Support, U.S. Gov't, P.H.S. (D013487) | Hemoglobins (Registry: 0, UI: D006454); Oxygen (Registry: S88TT14065, UI: D010100) | Acidosis (UI: D000138, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Alkalosis (UI: D000471, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Anemia (UI: D000740, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Anemia, Sickle Cell (UI: D000755, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Blood Specimen Collection (UI: D001800, Major: Yes); Body Temperature (UI: D001831, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Female (UI: D005260, Major: No); Fetal Blood (UI: D005312, Major: No); Heart Failure (UI: D006333, Major: No) - Qualifiers: blood (UI: Q000097, Major: No); Hemoglobins (UI: D006454, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Male (UI: D008297, Major: No); Methods (UI: D008722, Major: No); Oxygen (UI: D010100, Major: No) - Qualifiers: blood (UI: Q000097, Major: Yes); Veins (UI: D014680, Major: No) | Acidosis|Alkalosis|Anemia|Anemia, Sickle Cell|Blood Specimen Collection|Body Temperature|Coronary Disease|Female|Fetal Blood|Heart Failure|Hemoglobins|Humans|Hydrogen-Ion Concentration|Male|Methods|Oxygen|Veins | blood (0)|blood (0)|blood (0)|blood (0)|||blood (0)|||blood (0)|metabolism (1)|||||blood (1)| | 0|0|0|0|1|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2019-07-04 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 4084; doi: 10.1111/j.1365-2141.1976.tb01878.x | Myocardial Ischemia | ['Coronary Disease'] |
4,177 | 1 | [Case of congenital megaurethra associated with bilateral renal hyperplasia]. | MEDLINE | Manual | NLM | Authors report a very rare malformation of the external genital organs in a male new-born who died 48 hours after birth. This malformation consisted in a total aplasia of the corpus cavernosum and bulbus penis with a fusiforme dilatation of the anterior urethra. The malformation was associated with an anal imperforation, bilateral cryptorchidism and renal hypoplasia. | Bulletin de l'Association des anatomistes | 0376-6160 | Print | 59 | 166 | Print | 1,975 | Sep | null | 591-600 | M Colas (M); B Lauras (B); A Morin (A); J Cuilleret (J) | Case Reports (D002363); English Abstract (D004740); Journal Article (D016428) | null | Abnormalities, Multiple (UI: D000015, Major: Yes); Anus, Imperforate (UI: D001006, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Cryptorchidism (UI: D003456, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Heart Defects, Congenital (UI: D006330, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Humans (UI: D006801, Major: No); Infant, Newborn (UI: D007231, Major: No); Infant, Premature (UI: D007234, Major: No); Infant, Premature, Diseases (UI: D007235, Major: Yes); Kidney (UI: D007668, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: Yes); Male (UI: D008297, Major: No); Penis (UI: D010413, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: No); Urethra (UI: D014521, Major: No) - Qualifiers: abnormalities (UI: Q000002, Major: Yes) | Abnormalities, Multiple|Anus, Imperforate|Cryptorchidism|Heart Defects, Congenital|Humans|Infant, Newborn|Infant, Premature|Infant, Premature, Diseases|Kidney|Male|Penis|Urethra | |complications (0)|complications (0)|complications (0)|||||abnormalities (1)||abnormalities (0)|abnormalities (1) | 1|0|0|0|0|0|0|1|0|0|0|0 | null | 1976-07-06 | 2006-11-15 | pubmed: 1975-9-1; medline: 1975-9-1 0:1; entrez: 1975-9-1 0:0 | pubmed: 4177 | Heart Defects, Congenital | [] |
4,256 | 1 | Acebultolol: basis for the prediction of effect on exercise tolerance. | MEDLINE | Manual | NLM | Twelve unselected males suffering from documented coronary insufficiency and moderately severe angina submitted to graded multistage treadmill exercise testing on 3 separate days, 3.5 hr after a single dose of 0,200, or 400 mg of acebulolol, a cardioselective beta blocker. Control measures included random allocation of 2 patients to each of 6 balanced sequences of administration, standardized double-blind conditions, and variance analysis for Latin-square design with repeated measures on each subject. Performance was evaluated by measuring time elapsed until anginal pain, peak heart rate, peak product of heart rate and blood pressure, and peak oxygen consumption. Mean values for all criteria were significantly atered by 400 mg of acebutolol. Seven out of twelve patients were classified as responders (i.e., exercise duration increased 100% or more). The response after acebutolol was correlated with the performance on placebo in the base of exercise duration, peak heart rate, and peak product of heart rate and blood pressure. It is concluded that: (1) performance criteria are useful predictors of response to beta blockade and (2) acebutolol is a potent antianginal agent when judged by an objective treadmill exercise test. | Clinical pharmacology and therapeutics | 0009-9236 | Print | 19 | 3 | Print | 1,976 | Mar | null | 333-8 | P Biron (P); G Tremblay (G) | Clinical Trial (D016430); Journal Article (D016428); Randomized Controlled Trial (D016449) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Acebutolol (Registry: 67P356D8GH, UI: D000070) | Acebutolol (UI: D000070, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: Yes); Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: pharmacology (UI: Q000494, Major: No); Adult (UI: D000328, Major: No); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: No); Blood Pressure (UI: D001794, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: Yes); Exercise Test (UI: D005080, Major: Yes); Heart Rate (UI: D006339, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Humans (UI: D006801, Major: No); Middle Aged (UI: D008875, Major: No); Oxygen Consumption (UI: D010101, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Physical Exertion (UI: D005082, Major: No); Time Factors (UI: D013997, Major: No) | Acebutolol|Adrenergic beta-Antagonists|Adult|Angina Pectoris|Blood Pressure|Coronary Disease|Exercise Test|Heart Rate|Humans|Middle Aged|Oxygen Consumption|Physical Exertion|Time Factors | pharmacology (1)|pharmacology (0)||physiopathology (0)|drug effects (0)|physiopathology (1)||drug effects (0)|||drug effects (0)|| | 0|0|0|0|0|0|1|0|0|0|0|0|0 | null | 1976-07-06 | 2019-05-09 | pubmed: 1976-3-1; medline: 1976-3-1 0:1; entrez: 1976-3-1 0:0 | pubmed: 4256; doi: 10.1002/cpt1976193333 | Myocardial Ischemia | ['Angina Pectoris', 'Coronary Disease'] |
4,288 | 1 | The difficult hypertensive. | MEDLINE | Manual | NLM | With the wide range of medications available today it should be possible to obtain satisfactory control in the majority of hypertensive patients. However, there are various categories of patients who may present particular problems in management, as for example patients with cerebro-vascular and coronary disease, or with renal failure. A particularly important group is those presenting with severe resistant hypertension, and these patients may constitute about 5 to 10% of the hypertensive population. Considerations relevant to the management of patients presenting with such problems are discussed. Combined drug regimens employing clonidine or beta-blockers with peripheral vasodilators appear to be particularly useful. | Drugs | 0012-6667 | Print | 11 | 1 | Print | 1,976 | null | null | 55-60 | J Raftos (J) | Journal Article (D016428); Review (D016454) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Antihypertensive Agents (Registry: 0, UI: D000959); Diuretics (Registry: 0, UI: D004232); Vasodilator Agents (Registry: 0, UI: D014665) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Alcoholism (UI: D000437, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Antihypertensive Agents (UI: D000959, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Cerebrovascular Disorders (UI: D002561, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Coronary Disease (UI: D003327, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Depression (UI: D003863, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Diuretics (UI: D004232, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Drug Resistance (UI: D004351, Major: No); Drug Therapy, Combination (UI: D004359, Major: No); Emotions (UI: D004644, Major: No); Humans (UI: D006801, Major: No); Hypertension (UI: D006973, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); diagnosis (UI: Q000175, Major: No); drug therapy (UI: Q000188, Major: No); therapy (UI: Q000628, Major: Yes); Stress, Physiological (UI: D013312, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Substance-Related Disorders (UI: D019966, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Vasodilator Agents (UI: D014665, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No) | Adrenergic beta-Antagonists|Alcoholism|Antihypertensive Agents|Cerebrovascular Disorders|Coronary Disease|Depression|Diuretics|Drug Resistance|Drug Therapy, Combination|Emotions|Humans|Hypertension|Stress, Physiological|Substance-Related Disorders|Vasodilator Agents | therapeutic use (0)|complications (0)|therapeutic use (0)|complications (0)|complications (0)|complications (0)|therapeutic use (0)|||||complications (0); diagnosis (0); drug therapy (0); therapy (1)|complications (0)|complications (0)|therapeutic use (0) | 0|0|0|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2018-10-25 | pubmed: 1976-1-1; medline: 1976-1-1 0:1; entrez: 1976-1-1 0:0 | pubmed: 4288; doi: 10.2165/00003495-197611010-00005 | Cerebrovascular Disorders | ['Cerebrovascular Disorders'] |
4,649 | 1 | Morphologic and biochemical changes in autolysing dog heart muscle. | MEDLINE | Manual | NLM | The progressive changes in pH, lactate content, and light and electron microscopic appearances were studied in dog myocardium undergoing a 6-hour period of autolysis in vitro at 37 degrees C. and at room temperature. At 37 degrees C. there was a rapid cumulative fall in pH during the 1st hour after excision of the heart and a corresponding increase in lactate content, but little additional change in either subsequently. The nature and sequence of the morphologic alterations at this temperature were generally similar to those which occur in ischemic myocardium in vivo. At room temperature, a much slower cumulative decrease in pH and increase in lactate content took place throughout the whole period of investigation and was paralleled by a slower rate of development of morphologic change. | Laboratory investigation; a journal of technical methods and pathology | 0023-6837 | Print | 34 | 4 | Print | 1,976 | Apr | null | 357-62 | L C Armiger (LC); R N Seelye (RN); V M Carnell (VM); C U Smith (CU); J B Gavin (JB); P B Herdson (PB) | Journal Article (D016428) | Lactates (Registry: 0, UI: D007773); Glycogen (Registry: 9005-79-2, UI: D006003) | Animals (UI: D000818, Major: No); Autolysis (UI: D001329, Major: Yes); Dogs (UI: D004285, Major: No); Glycogen (UI: D006003, Major: No) - Qualifiers: analysis (UI: Q000032, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Lactates (UI: D007773, Major: No) - Qualifiers: analysis (UI: Q000032, Major: No); Mitochondria (UI: D008928, Major: No) - Qualifiers: ultrastructure (UI: Q000648, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: pathology (UI: Q000473, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: analysis (UI: Q000032, Major: No); pathology (UI: Q000473, Major: Yes); ultrastructure (UI: Q000648, Major: No); Myofibrils (UI: D009210, Major: No) - Qualifiers: ultrastructure (UI: Q000648, Major: No) | Animals|Autolysis|Dogs|Glycogen|Hydrogen-Ion Concentration|Lactates|Mitochondria|Myocardial Infarction|Myocardium|Myofibrils | |||analysis (0)||analysis (0)|ultrastructure (0)|pathology (0)|analysis (0); pathology (1); ultrastructure (0)|ultrastructure (0) | 0|1|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2003-11-14 | pubmed: 1976-4-1; medline: 1976-4-1 0:1; entrez: 1976-4-1 0:0 | pubmed: 4649 | Myocardial Ischemia | ['Myocardial Infarction'] |
4,779 | 1 | Atherosclerotic cerebral infarction: pathophysiologic aspects. | MEDLINE | Manual | NLM | When the supply of substrate to the brain is threatened, homeostatic mechanisms induce cerebral vasodilatation to compensate for the insufficiency. When a region of the brain is rendered completely ischemic, local infarction occurs. The size of the infarct depends partly on the availability of collateral circulation and the adequacy of the homeostatic mechanisms controlling blood flow in stillpatent vessels. Several approaches to acute-phase treatment of stroke derive from clinical and experimental studies of cerebral blood flow and metabolism. We must conclude that both surgical and nonsurgical therapeutic measures have been of limited value in the treatment of cerebral infarction and that the basic therapy for completed stroke remains good medical management of complications and attentive nursing care. | Postgraduate medicine | 0032-5481 | Print | 59 | 3 | Print | 1,976 | Mar | null | 115-8 | J J Caronna (JJ); F H McDowell (FH) | Journal Article (D016428) | null | Blood Flow Velocity (UI: D001783, Major: No); Brain (UI: D001921, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: Yes); Brain Edema (UI: D001929, Major: No) - Qualifiers: etiology (UI: Q000209, Major: No); therapy (UI: Q000628, Major: No); Cerebrovascular Circulation (UI: D002560, Major: Yes); Cerebrovascular Disorders (UI: D002561, Major: No) - Qualifiers: physiopathology (UI: Q000503, Major: Yes); prevention & control (UI: Q000517, Major: No); therapy (UI: Q000628, Major: No); Energy Metabolism (UI: D004734, Major: No); Humans (UI: D006801, Major: No); Hydrogen-Ion Concentration (UI: D006863, Major: No); Hypertension (UI: D006973, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Oxygen Consumption (UI: D010101, Major: No); Regional Blood Flow (UI: D012039, Major: No); Time Factors (UI: D013997, Major: No) | Blood Flow Velocity|Brain|Brain Edema|Cerebrovascular Circulation|Cerebrovascular Disorders|Energy Metabolism|Humans|Hydrogen-Ion Concentration|Hypertension|Oxygen Consumption|Regional Blood Flow|Time Factors | |metabolism (1)|etiology (0); therapy (0)||physiopathology (1); prevention & control (0); therapy (0)||||complications (0)||| | 0|0|0|1|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2019-07-13 | pubmed: 1976-3-1; medline: 1976-3-1 0:1; entrez: 1976-3-1 0:0 | pubmed: 4779; doi: 10.1080/00325481.1976.11714300 | Cerebrovascular Disorders | ['Cerebrovascular Disorders'] |
4,782 | 1 | Myocardial ischemia from coronary arterial spasm. | MEDLINE | Manual | NLM | Spasm of coronary arteries can cause chest pain indistinguishable from classic angina pectoris in patients without atherosclerosis of these vessels or recognizable heart disease. Associated electrocardiographic changes usually correspond to the coronary artery affected and disappear when the attack of pain ends. Sublingual nitrates are excellent agents for the control of the episodic anginal symptoms. There have been scattered reports of myocardial infarction occurring in patients with normal coronary arteries; a role of arterial spasm in these cases in speculative. | Postgraduate medicine | 0032-5481 | Print | 59 | 4 | Print | 1,976 | Apr | null | 207-11 | S J Gulotta (SJ); K Geller (K) | Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); drug therapy (UI: Q000188, Major: No); etiology (UI: Q000209, Major: Yes); Coronary Vessels (UI: D003331, Major: Yes); Electrocardiography (UI: D004562, Major: No); Female (UI: D005260, Major: No); Humans (UI: D006801, Major: No); Male (UI: D008297, Major: No); Middle Aged (UI: D008875, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: etiology (UI: Q000209, Major: No); Spasm (UI: D013035, Major: No) - Qualifiers: complications (UI: Q000150, Major: Yes); diagnosis (UI: Q000175, Major: No); drug therapy (UI: Q000188, Major: No) | Adrenergic beta-Antagonists|Angina Pectoris|Coronary Vessels|Electrocardiography|Female|Humans|Male|Middle Aged|Myocardial Infarction|Spasm | therapeutic use (0)|diagnosis (0); drug therapy (0); etiology (1)|||||||etiology (0)|complications (1); diagnosis (0); drug therapy (0) | 0|0|1|0|0|0|0|0|0|0 | null | 1976-07-06 | 2019-07-13 | pubmed: 1976-4-1; medline: 1976-4-1 0:1; entrez: 1976-4-1 0:0 | pubmed: 4782; doi: 10.1080/00325481.1976.11714341 | Myocardial Ischemia | ['Angina Pectoris', 'Myocardial Infarction'] |
4,783 | 1 | Angina pectoris. Diagnosis and treatment. | MEDLINE | Manual | NLM | The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook. | Postgraduate medicine | 0032-5481 | Print | 59 | 5 | Print | 1,976 | May | null | 179-88 | R Zelis (R); J A Liedtke (JA); D M Leaman (DM); J D Babb (JD); B H Roberts (BH) | Journal Article (D016428) | Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Digitalis Glycosides (Registry: 0, UI: D004071); Ethanol (Registry: 3K9958V90M, UI: D000431); Nitroglycerin (Registry: G59M7S0WS3, UI: D005996) | Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Angina Pectoris (UI: D000787, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); etiology (UI: Q000209, Major: No); therapy (UI: Q000628, Major: Yes); Coronary Disease (UI: D003327, Major: No) - Qualifiers: complications (UI: Q000150, Major: No); Diagnosis, Differential (UI: D003937, Major: No); Digitalis Glycosides (UI: D004071, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Ethanol (UI: D000431, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Exercise Therapy (UI: D005081, Major: No); Humans (UI: D006801, Major: No); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Nitroglycerin (UI: D005996, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Oxygen Consumption (UI: D010101, Major: No); Pain (UI: D010146, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No) | Adrenergic beta-Antagonists|Angina Pectoris|Coronary Disease|Diagnosis, Differential|Digitalis Glycosides|Ethanol|Exercise Therapy|Humans|Myocardium|Nitroglycerin|Oxygen Consumption|Pain | therapeutic use (0)|diagnosis (0); etiology (0); therapy (1)|complications (0)||therapeutic use (0)|therapeutic use (0)|||metabolism (0)|therapeutic use (0)||diagnosis (0) | 0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2019-07-13 | pubmed: 1976-5-1; medline: 1976-5-1 0:1; entrez: 1976-5-1 0:0 | pubmed: 4783; doi: 10.1080/00325481.1976.11714365 | Myocardial Ischemia | ['Angina Pectoris', 'Coronary Disease'] |
4,787 | 1 | [Congenital heart malformations in neonates, infants and young children (author's transl)]. | MEDLINE | Manual | NLM | Congenital heart malformations in neonates, infants and young children represent the main problem of paediatric cardiology in Poland. Congenital cardiovascular diseases (incidence also approximately 8 per 1000 in liveborn infants) cause very high mortality, particularly in the neonatal and infantile period. Approximately 5000 live-born children are affected every year by serious heart malformations. For at least two thirds of these previously hopelessly ill infants there are real possibilities of effective medical and surgical treatment. Not only a considerable drop in mortality in the earliest infancy would be achieved, but: a further normal physical and psychical growth and development of these children would be possible. At present, however, the available possibilities are by far not sufficient, as in all hitherto functioning centres we were able to manage 200-300 children yearly, whereas the real needs are at leasttenfold greater. Therefore it is necessary to: Increase the number and capacity of hospital wards capable enough to provide the intensive cardiopulmonary care; to execute appropriate reorganization aimed to concentrating the appropriate specialists (pediatric cardiologists, radiologists, surgeons, anesthesiologists, nurses) and equipment (cardiological and cardiosurgical appliances, X-ray equipment, intensive care units etc.) in centres designated for the above tasks. At least 7 paediatric intensive care and cardiosurgical centres should be instituted in Poland for a satisfactory management of congenital heart diseases. | Problemy medycyny wieku rozwojowego | 0303-2264 | Print | 5 | null | Print | 1,975 | null | null | 191-2 | J Swiderski (J) | Congress (D016423) | null | Age Factors (UI: D000367, Major: No); Child, Preschool (UI: D002675, Major: No); Congresses as Topic (UI: D003226, Major: No); Heart Defects, Congenital (UI: D006330, Major: No) - Qualifiers: diagnosis (UI: Q000175, Major: No); surgery (UI: Q000601, Major: No); therapy (UI: Q000628, Major: Yes); Humans (UI: D006801, Major: No); Infant (UI: D007223, Major: No); Infant, Newborn (UI: D007231, Major: No); Poland (UI: D011044, Major: No) | Age Factors|Child, Preschool|Congresses as Topic|Heart Defects, Congenital|Humans|Infant|Infant, Newborn|Poland | |||diagnosis (0); surgery (0); therapy (1)|||| | 0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2018-12-03 | pubmed: 1975-1-1; medline: 1975-1-1 0:1; entrez: 1975-1-1 0:0 | pubmed: 4787 | Heart Defects, Congenital | [] |
4,896 | 1 | Reduction in myocardial infarct size: prevention of heart cell death. | MEDLINE | Manual | NLM | The course of myocardial necrosis, the clinical syndrome, and methods of treatment are presented. Heart cell death may be prevented by maintaining the balance between myocardial oxygen and energy supply and consumption. New technics of improving this balance by reducing myocardial energy demand, altering metabolism, increasing myocardial substrate supply, and protecting cellular integrity are discussed. | Southern medical journal | 0038-4348 | Print | 69 | 4 | Print | 1,976 | Apr | null | 442-8 | R J Kones (RJ); J H Phillips (JH) | Journal Article (D016428) | Adrenal Cortex Hormones (Registry: 0, UI: D000305); Adrenergic beta-Antagonists (Registry: 0, UI: D000319); Insulin (Registry: 0, UI: D007328); Vasodilator Agents (Registry: 0, UI: D014665); Hyaluronoglucosaminidase (Registry: EC 3.2.1.35, UI: D006821); Glucose (Registry: IY9XDZ35W2, UI: D005947); Potassium (Registry: RWP5GA015D, UI: D011188) | Adrenal Cortex Hormones (UI: D000305, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Adrenergic beta-Antagonists (UI: D000319, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Assisted Circulation (UI: D001243, Major: No); Autolysis (UI: D001329, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); Cardiac Output (UI: D002302, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Coronary Circulation (UI: D003326, Major: No); Energy Metabolism (UI: D004734, Major: Yes); Energy Transfer (UI: D004735, Major: No) - Qualifiers: drug effects (UI: Q000187, Major: No); Glucose (UI: D005947, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Humans (UI: D006801, Major: No); Hyaluronoglucosaminidase (UI: D006821, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No); Insulin (UI: D007328, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Myocardial Infarction (UI: D009203, Major: No) - Qualifiers: drug therapy (UI: Q000188, Major: No); metabolism (UI: Q000378, Major: No); pathology (UI: Q000473, Major: Yes); Myocardium (UI: D009206, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); pathology (UI: Q000473, Major: Yes); Necrosis (UI: D009336, Major: No); Oxygen Consumption (UI: D010101, Major: No); Perfusion (UI: D010477, Major: No); Potassium (UI: D011188, Major: No) - Qualifiers: metabolism (UI: Q000378, Major: No); Vasodilator Agents (UI: D014665, Major: No) - Qualifiers: therapeutic use (UI: Q000627, Major: No) | Adrenal Cortex Hormones|Adrenergic beta-Antagonists|Assisted Circulation|Autolysis|Cardiac Output|Coronary Circulation|Energy Metabolism|Energy Transfer|Glucose|Humans|Hyaluronoglucosaminidase|Insulin|Myocardial Infarction|Myocardium|Necrosis|Oxygen Consumption|Perfusion|Potassium|Vasodilator Agents | therapeutic use (0)|therapeutic use (0)||drug therapy (0)|drug effects (0)|||drug effects (0)|metabolism (0)||therapeutic use (0)|metabolism (0)|drug therapy (0); metabolism (0); pathology (1)|metabolism (0); pathology (1)||||metabolism (0)|therapeutic use (0) | 0|0|0|0|0|0|1|0|0|0|0|0|0|0|0|0|0|0|0 | null | 1976-07-06 | 2019-07-02 | pubmed: 1976-4-1; medline: 1976-4-1 0:1; entrez: 1976-4-1 0:0 | pubmed: 4896; doi: 10.1097/00007611-197604000-00020 | Myocardial Ischemia | ['Myocardial Infarction'] |
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1 Dataset Collection
1.1 Name: PubMed25 Cardio
1.2 Cardio Mesh Descriptors (Parents)
- Cerebrovascular Disorders
- Myocardial Ischemia
- Cardiomyopathies
- Arrhythmias, Cardiac
- Heart Valve Diseases
- Heart Defects, Congenital
We thank and acknowledge the contribution of Prof. David Liem for creating and providing the mesh descriptors tree for Cardiovascular Diseases.
1.3 Curation Process
- We downloaded raw xml files from pubmed25
- Total files: 1274 (filename example: pubmed25n0001.xml)
- Total Articles: 38,202,567 (38M)
- We filter articles with abstracts that has matching MeSH Descriptions with Cardio Mesh Descriptors mentioned above
1.4 PubMed 25 Cardio Analytics
- Total Cardio Related Articles: 864244
- Top Journal: The American journal of cardiology (19779 articles)
- More details are covered in the pubmed25_cardio_analytics
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